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Structure And Function 1 > Exam 2 > Flashcards

Exam 2 Flashcards

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1
Q

Name the basic tissue type

  • Sheets of cells covering a surface or lining a cavity
  • responsible for the major function of most organs
A

EPITHELIUM

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2
Q

Name the basic tissue type

  • Cells and ECM (extracellular matrix) that support and connect other basic tissue in organs
  • Includes bone/cartilage/blood
A

CONNECTIVE TISSUE

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3
Q

Name the basic tissue type

-contractile tissues

A

MUSCLE

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4
Q

Name the basic tissue type

-Conductive tissues that distribute signals that control various body functions

A

NERVOUS TISSUE

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5
Q

Nervous system is divided into what? Further division?

A

1) CNS - central nervous system (Brain and Spinal cord)

2) PNS- peripheral nervous system (cranial, spinal and peripheral nerves)
* *Afferent - brings SENSORY info (about touch, taste, smell, sight and sound) from the periphery TOWARD the CNS
* *Efferent- carries MOTOR info to the periphery FROM the CNS

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6
Q

What are the 2 main cells if the CNS and their function? How are these 2 cells further classified?

A

1) Neurons - conducting cells (classified based on number of dendrites and axons
* MULTIPOLAR. *UNIPOLAR. *BIPOLAR

2) Glia - non-neuronal supporting cells with different functions
(Smaller than neurons with dark staining nuclei, highly branch, DO NOT CONDUCT)
* ASTROCYTES
*OLIGODENDROCYTES
*EPENDYMAL CELLS
*MICROGLIA

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7
Q

What are the 3 parts of a Neuron?

A

SOMA
AXON
DENDRITES

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8
Q

Name the part of a neuron

-can be a few or many branched processes that RECEIVE SIGNALS
Smaller branches are spines where synapses form

A

DENDRITES
**smaller branches on dendrites are DENDRITIC SPINES where SYNAPSES with axons form (the branches INCREASE surface area available for synapse)

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9
Q

What can be found in a neuron SOMA

A

Cell body (perikaryon) containing cytoplasmic organelles

  • LARGE nucleus with prominent nucleolus
  • MANY dark staining basophils NISSL BODIES (areas of RER and polyribosomes)
  • Golgi, mitochondria, lysosomes, microtubules and neurofilaments
  • LIPOFUSCIN- yellow pigment granules
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10
Q

Name the part of a neuron

  • long process extending from pole opposite dendrites which CONDUCT SIGNAL as an action potential to a target cell (either another neuron or a muscle)
  • Has a hillock near the start and a terminal at the end
A

AXON

Axon HILLOCK- clear area of CELL BODY, NO NISSL BODIES, near the start of the axon

Axon TERMINAL- small branches at the end of the axon that MAKE SYNAPTIC CONTACT with the target cell

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11
Q

How many types of atonal transport do we have? What are they?

A

2 types
FAST axonal transport (Anterograde and Retrograde)
SLOW axonal transport (ANTEROGRADE ONLY)

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12
Q

Name the axonal transport

  • toward the axon TERMINAL
  • 100-400 mm/day
  • uses KINESIN
  • Vesicles that bud from the golgi can be used as (precursors for NTs, enzymes that make small NTs, plasma membrane proteins)
  • Mitochondria
  • Tracers (to see where cell body is/target)
A

FAST Axonal Transport - ANTEROGRADE

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13
Q

Name the Axonal transport

  • toward the CELL BODY
  • 50-200 mm/day
  • uses DYNEIN
  • Has ENDOCYTIC VESICLES (trophies factors e.g NGF)
  • Mitochondria
  • Viruses and toxins (herpes simplex, rabies, polio, tetanus toxin)
  • Tracers
A

FAST Axonal Transport - RETROGRADE

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14
Q

Name the Axonal Transport

  • 0.2-0.4 mm/day
  • toward the AXON TERMINAL
  • HAs CYTOSKELETAL PROTEINS (tubular, actin, neurofilaments)
  • Has CYTOPLASMIC PROTEINS (Enzymes, calmodulin)
A

SLOW Axonal Transport - ANTEROGRADE

** Slow axonal transport has ONLY ANTEROGRADE direction (move TOWARD the AXON TERMINAL)

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15
Q

Axon terminal of a presynaptic cell is filled with what that contains what?
What can these perform?
What are the targets?

A
  • Synaptic vesicles that contain Neurotransmitters
  • Perform SYNAPSE
  • Targets may be other neurons, muscles or glands
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16
Q

Name the types of neurons based on number of dendrites and axons and GIVE EXAMPLES

1) NUMEROUS branched DENDRITES, SINGLE AXON
2) SINGLE DENDRITE, SINGLE AXON
3) SINGLE BIDIRECTIONAL AXON

A

1) MULTIPOLAR (All motor neurons and interneurons)
2) BIPOLAR (sensory neurons found in eye, ear, olfactory epithelium)
3) UNIPOLAR/pseudounipolar
* * originally bipolar during development
* * one branch to CNS, other to PERIPHERY
* * cell bodies of SENSORY neurons found in GANGLIA

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17
Q

Tell me about the origin(s) of GLIAL in the CNS

What are the origins of the respective glial cells?

A

2 MAIN ORIGINS

1) Derived from NEUROEPITHELIAL stem cells
* Oligodendrocytes - produce myelin in the CNS (smaller than astrocytes)
* Astrocytes - Protoplasmic (found in gray matter) and Fibrous (found in white matter)
* Ependymal cells

2) Derived from MONOCYTES
* Microglia- phagocytosis cells similar to macrophages (clean up debris)

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18
Q

The plasma membrane of SUPPORTING CELLS form a PROTECTIVE INSULATION in CNS and PNS.

What is this protective insulation called?
What supporting cells form this in CNS and PNS respectively?

There are GAPS in this protective insulation where adjacent cell processes meet.
What are these gaps called? Function?

A

MYELIN SHEATH

CNS- Oligodendrocytes (myelinate numerous axons)
PNS- Schwann cells (myelinate individual axon)

NODES OF RANVIER - gaps in the myelin sheath where adjacent cell processes meet (propagate AP down the axon length)

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19
Q

Name the Nodes of Ranvier

  • region btw adjacent myelin sheaths
  • region where cytoplasmic loops of myelinating cell overlap next to the node
  • region adjacent to the paranode
  • region btw juxtaparanodes of a single myelin sheath

What is the format/arrangement

A

NODE
PARANODE
JUXTAPARANODE
INTERNODE

** Regions have concentrations of specific ion channels and transporters

IJP-N-PJI (format)

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20
Q

Compare myelination in CNS vs PNS

Unmyelinated axons in PNS?

A

CNS
—Oligodendrocytes myelinate multiple axons
-Nodes “open”, but may be in contact with astrocytes
-No basal lamina

PNS

  • Schwann cell myelinates single axon
  • Schwann cell protrusions overlap nodes
  • Schwann cell rests on BASAL LAMINA
  • Schwann cells can also envelope MULTIPLE UNMYELINATED axons
  • Schwann cells enveloping both the myelinated and unmyelinated axons are surrounded by BASAL LAMINA
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21
Q

Name the glial supporting cell

  • Largest and most abundant glial cell
  • many processes give a STAR shaped appearance
  • Large OVAL NUCLEUS
  • express the intermediate filament protein GFAP
  • END FEET CONTACT - (capillaries and the inner surface of the pia mater, areas of neurons without myelin)
  • Control the environment surrounding neurons (part of the BLOOD-BRAIN BARRIER, nutritional support, NT uptake (potassium and glutamate), electrolyte balance)
A

ASTROCYTES

    • In response to injury, cells divide and form scar tissue
  • *Form the GLIA LIMITANS
  • glia limiting membrane
  • impermeable barrier formed by branched processes of astrocytes extending to the basal lamina of the pia mater
  • surrounds the brain and the spinal cord
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22
Q

Name the glial cell

  • Simple CUBOIDAL To COLUMNAR epithelial cells lining the ventricles of the brain and the central canal of the spinal cord
  • Cilia and microvilli on the apical surface
  • DESMOSOMES btw adjacent cells
  • Basal processes may contact blood vessels or astrocytes
A

EPENDYMAL CELLS

  • *Cilia- facilitate movement of CSF through central canal of spinal cord
  • *Microvilli- may have some absorptive functions
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23
Q

Name the glial cell

-Derived form monocytes that migrate to the brain
(Respond to tissue injury and participate in immune response, PHAGOCYTIC)
-SMALLEST glial cells with IRREGULAR SHAPE and dark staining nucleus

A

MICROGLIA

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24
Q

Describe Neuronal Degeneration and the events that occur in the CELL BODY, DISTAL AXON, PROXIMAL AXON

A

CELL BODY

  • swelling displaces nucleus to periphery
  • chromatolysis (dispersion of nissl substances to periphery0

DISTAL AXON (Wallerian degeneration)

  • loss of connection to cell body
  • Degeneration
  • removal of debris
  • scar formation

PROXIMAL AXON

  • maintains connection to cell body
  • Degeneration back 2-3 internodes
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25
During neuronal DEGENERATION : What Removes debris in CNS and PNS? What cause Scar formation in CNS and PNS?
Removal of debris CNS - MICROGLIA PNS - MACROPHAGES Scar formation CNS- fibrous ASTROCYTES proliferate PNS- FIBROBLASTS form scar
26
Tell me about Neuronal REGENERATION in CNS and PNS respectively What prevents regrowth of axon in CNS? What 2 things help direct axonal sprouts to correct target in PNS? What is the name of the AXONS that were not able to find their way to the proper sheath to connect to target? PAINFUL when irritated?
CNS -scar formed by astrocytes prevents regrowth of axon PNS -ENDONEURIAL SHEATH (in intact) and SCHWANN cells act as a quite for directing axonal sprouts to correct targets (laminin and growth factors) -proliferation of Schwann cells and myelinization of regrowing axon -eventual reconnection to target NEUROMA (Severed ends too widely separated, scar forms barrier)
27
The CNS is composed of Gray and White mater. Differentiate btw the 2 Which has NEUROPIL? Which has NO NEURONAL CELL BODIES? Which has unmyelinated vs myelinated axons?
GRAY MATTER - OUTER surface of the cerebrum and cerebellum - central region of the spinal cord - consist of ; NEURONS (cell bodies and dendrites), UNMYELINATED AXONS, Neuroglia - NEUROPIL -densely packed region of cell processes WHITE MATTER - Primarily; MYELINATED AXONS (some unmyelinated axons), Oligodendrocytes, blood vessels - NO NEURONAL CELL BODIES
28
Brain is made up of Meninges Cerebral Cortex Cerebellum Which is the connective tissue coverings of the brain and the spinal cord? What are the layers? What are the CT types for the different layers? Which layer is adjacent to nervous tissue? What acts as shock absorber?
MENINGES Layers 1) DURA MATER - outer covering of DENSE connective tissue 2) ARACHNOID MATER- middle layer of LESS DENSE CT * *Has the Sub-arachnoid space (Network of collagen and elastin fibers filled with CSF that acts as SHOCK ABSORBER) 3) PIA MATER - Inner layer ADJACENT TO NERVOUS TISSUE of LOOSE CT (carries blood vessels)
29
Brain is made up of Meninges Cerebral Cortex Cerebellum Which has Gray matter, white matter and PYRAMIDAL NEURONS? Gray matter is composed of how many layers of cells? What are they? WHat is the Outermost/Innermost layer Which has myelinated axons? WHere does the name pyramidal come from?
``` CEREBRAL CORTEX 1) Gray matter -composed of 6 layers of cells **a) molecular layer -OUTERMOST, external granular layer, external pyramidal layer, Internal granular layer, Internal pyramidal layer, **f) multiform layer -INNERMOST -contains many neurons and glia ``` 2) White matter - internal to the gray matter - composed of MYELINATED AXONS 3) PYRAMIDAL NEURONS - smaller ones in external pyramidal layer - larger ones in internal pyramidal layer - NAME from PYRAMIDAL SHAPE of the cell body - dendrites project toward surface - Axons extend into the white matter
30
Brain is made up of Meninges Cerebral Cortex Cerebellum Which has molecular, PURKINJE and granular layer?
CEREBELLUM 3 layers 1) Molecular- OUTERMOST, mostly fibers and a few neurons 2) PURKINJE -middle * *Purkinje cells (most prominent cell, large cell bodies in a single layer btw the molecular and granular layers, extensively branched dendrites into molecular layer) 3) Granular- Inner, MANY SMALL NEURONS
31
Orientation of Gray and White mater in SPINAL CORD? How is this different from the brain? What does dorsal and central horn of spinal cord contain?
SPINAL CORD Silver staining Gray matter - lighter in color (yellow) - MORE INSIDE - CENTRAL CANAL White matter - darker in color (brown) - MORE OUTER- contains ascending and descending myelinated axons and glia Posterior/DORSAL horn- SENSORY fibers of DORSAL ROOT GANGLION Anterior/Ventral horn - Cell bodies and fibers of MOTOR NERVES BRAIN/CEREBRAL CORTEX Gray mater- MORE OUTSIDE White Mater- MORE INSIDE
32
The nerves and supporting cells that are found outside the CNS are called? What is this system made up of?
PNS - Peripheral Nervous System -Made of cranial and spinal nerves and associated ganglia
33
NAme the layer(s)of Peripheral Nerves - DENSE CT layer that surround the peripheral nerves and BINDS MULTIPLE FASCICLES together - THINNER LAYER of CT that surround the BUDLES of AXONS(fascicles) - THIN LAYER of LOSSE CT that surround EACH AXON and its associated SCHWANN CELL
EPINEURIUM PERINEURIUM ENDONEURIUM (vascular CT layer)
34
Enteric ganglia of PNS is made up of what plexus?
1) AUERBACH’s plexus - Myenteric (found btw the two layers of the muscularis externa) 2)MEISNER’s Plexus **controls motility and secretion in the intestinal tract
35
Skin sensory receptors are composed of; Free nerve endings, market discs, Krause end bulbs, root hair plexus, MEISSNER corpuscles, PACINIAN corpuscles, ruffing endings Which are receptive to touch?
``` Markel discs Krause end bulbs Root hair plexus MEISSNER corpuscles **First 4 are TOUCH ONLY ``` PACINIAN corpuscles (pressure, vibration, touch)
36
Skin sensory receptors are composed of; Free nerve endings, market discs, Krause end bulbs, root hair plexus, MEISSNER corpuscles, PACINIAN corpuscles, ruffing endings Which are receptive to pressure?
PaCINIAN corpuscles (pressure, vibration, touch) Ruffini ending (ONLY PRESSURE)
37
Name the Skin sensory receptor - Receptive to TOUCH - Found in the DERMAL PAPILLA of THICK SKIN - Encapsulated
MEISSNER corpuscles
38
Name the skin sensory receptor - Receptive to PRESSuRE, vIbrATION, TOUCH - ONION appearance - Found in the HYPODERMIS of THICK Skin
PACINIAN Corpuscles
39
Name the sensory receptor Has - Muscle spindle - Golgi tendon organ
MUSCLE SENSORY RECEPTORS
40
Taste sensation is recognized by TASTE BUDS Taste buds are found in what types of PAPILLAE on the surface of the tongue ? What are all the types of papillae? All papillae is covered by what type of epithelium? Which papilla has no taste buds? Which is not well developed in humans?
4 Types of PAPILLAE 1) FILIFORM -entire surface of the tongue, small pointed with keratin at tip, NO TASTE BUDS, MOST NUMEROUS, smallest papillae 2) FUNGIFORM -anterior region and tip of tongue, TASTE BUDS found on APICAL surface of PAPILLA, MUSHROOM LIKE shape 3) CIRCUMVALLATE -posterior region, characterized by DEEP FURROW, multiple TASTE BUDS face the furrow 4) FOLIATE -posterior sides of tongue, TASTE BUDS on SIDES of PAPILLA, Not well developed in humans **All papillae covered in STRATIFIED SQUAMOUS EPITHELIUM
41
Taste bud structure? What 3 cells does it contain? How it works location of taste buds?
How it works TASTANTS -open pore, bind receptors n receptor cells , initiate a signal cascade, release chemical mediator that stimulate afferent nerves 3 CELLS 1) GUSTATORY/TASTE Cells - located with each taste bud, extend the base of the taste bud to the taste pore. Apex of each taste cell has MICROVLLI for absorption 2) SUSTENTACULAR cell 3) BASAL CELLS -undifferentiated, stem cells for the other 2 cells types in taste buds LOCATION Tongue (most numerous), soft palate, pharynx, epiglottis
42
COMponents of Olfaction receptors Does it have goblet cells? What has goblet cells? What are the cell types What is the CT that lines the olfactory epithelium called? What covers bone of olfactory region?
PSEUDO STRATIFIED olfactory epithelium - found on surface of SUPERIOR CONCHA, adjacent septum and roof of nasal cavity (NO GOBLET CELLS, NON MOTILE CILIA - function as ODOR receptor) CELL TYPES - Apical supportive - Olfactory cells (BIPOLAR NEURONS) - Basal cells - Transition to respiratory epithelium - **LAMINA PROPRIA -CT underlying epithelium , also covers bone of olfactory region
43
How does olfaction work through the LAMINA PROPRIA What secrete the serous fluid? What warms inspired air?
-UNMYELINATED nerve fibers carry axons of BIPOLAR NEURONS to olfactory bulb. -**The base of the olfactory cells convert to axons that leave the epithelium by continuing through the basement membrane, converge in the connective tissue below the epithelium to form bundle of nerve fibers that pass through the ethmoid bone of the skull, and synapse in the olfactory bulb of the brain (olfactory, or cranial nerve I). - BOWMAN’s GLAND- secrete serous fluid - dissolve odor so they can bind to receptors on the NON-MOTILE cilia of BIPOLAR NEURONS - BLOOD VESSELS- warm inspired air
44
Muscle fibers are composed of Skeletal, Cardiac and Smooth Muscle Name the muscle respectively: - A single long MULTINUCLEATED cell with FLATTENED NUCLEI on the periphery - An INDETERMINABLE number of cells joined end to end, each with 1 or 2 ROUNDED NUCLEI - A single cell with a SINGLE NUCLEUS in the CENTER
- SKELETAL - CARDIAC - SMOOTH
45
Name the Muscle -VOLUNTARY -Has Muscle fiber/cells made of bundles of MYOFIBRILS (grp of actin and myosin filaments) **SARCOPLASMIC RETICULUM (store calcium) -closely associated with group of MYOFIBRILS -Each fiber surrounded by layer of CT called ENDOMYSIUM -MOTOR END PLATES are the site of nerve innervations and transmission of stimuli to muscle -axon terminal of motor end plate has Neuromuscular Junctions /motor end plates with Ach NT. And AchE to inactive excess Ach
SKELETAL MUSCLE a
46
For SKELETAL MUSCLE, WHat is the Basic functional unit of a MYOFIBRILS? - composed of thick (myosin) and thin (actin) filaments and associated proteins - OVERLAPPING of filaments creates banding pattern of STRIATIONS What is this basic unit composed of ?
SARCOMERE **repeated units of sarcomere run the length of the muscle fiber ``` Structure has; Z to Z line I band A band H zone M line Muscle triad ``` **SARCOPLASMIC reticulum and MITOCHONDRIA surround each SARCOMERE
47
Name the sarcomere structure of SKELETAL MUSCLE (line, band, zone,triad etc) - SARCOMERE (the contractile unit) - point of attachment for the thin filaments (actin/pink) - bisects I Bands
Z line Z line to Z line (SARCOMERE- smallest contractile unit of muscle)
48
Name the sarcomere structure of SKELETAL MUSCLE (line, band, zone,triad etc) - light stripe - Z line and thin filaments (actin) - ALPHA-actinin protein binds actin filaments to Z line
I BAND - light stripe **shorten during contraction (also H zone)
49
Name the sarcomere structure OF SKELETAL MUSCLE (line, band, zone,triad etc) - dark stripe - represents the full length of the THICK filaments (myosin/blue) - Thin filaments overlap - TITIN PROTEIN anchors MYOSIN filaments to Z line **located in the MIDDLE of sarcomere
A BAND -dark stripe **stay same during contraction
50
Name the sarcomere structure of Skeletal muscle (line, band, zone,triad etc) - contains THICK filaments - SIZE CHANGES depending on the state of contraction of the muscle **on either side of M bands-contain only MYOSIN filaments
H zone/band **shorten during contraction (also I band)
51
Name the sarcomere structure of skeletal muscle (line, band, zone,triad etc) - anchor point of THICK filaments (MYOSIN) * *middle of A band-represents linkage of myosin filament
M line
52
Name the sarcomere structure of skeletal muscle(line, band, zone,triad etc) Located at the A-I junction - Made of expanded TERMNIAL CUSTERNAE of The SARCOPLASMIC reticulum (SR) and T tubules - T TUBULE is formed by sarcolemma invaginations into each myofiber
MUSCLE TRIAD **At each triad, the AP is transmitted from the T tubules to every MYOFIBER and MYOFIBRILS as well as the SR membrane
53
Skeletal Muscle Organization 1) Groups of several muscle fibers form ? 2) Muscle fibers are covered by ? 3) The outer covering of the fascicles is called the ? 4) Groups of fascicles form? 5) The muscle is covered with CT called the?
1) A Fascicle 2) ENDOMYSIUM 3) PERIMYSIUM 4) muscle 5) EPIMYSIUM
54
Connective tissue coverings allow penetration of blood vessels and nerves. What are the CT components of the SKELETAL MUSCLE ?
-TYPE 1 COLLAGEN - DENSE IRrEGULAR CT * EPIMYSIUM * PERIMYSIUM - LOOSE IRREGULAR CT * ENDOMYSIUM
55
CARDIAC muscle cells are joined by what dense junctional complexes to make a FIBER? What do these junctional complexes contain? Zig-zag appearance
INTERCALATED DISKS ** consist of fascia adherents, desmosomes and gap junction GAP junctions - allow for a rapid spread of stimuli throughout the entire muscle mass) - Couple all fibers for rhythmic contraction -FUNCTIONAL SYNCYTIUM (ion can diffuse through gap junctions allow contraction stimuli pass through entire muscle mass)
56
What are the 3 components of a CARDIAC SARCOMERE Conduction of excitatory impulses to the cardiac sarcomeres is through what component(s)?
1) T tubules -located at Z LINES make DIADS with SARCOPLASMIC reticulum 2) Sarcoplamic reticulum - less well developed, calcium is IMPORTED from outside the cardiac muscle into the SARCOPLASM for contraction 3) Mitochondria - larger and more ABUNDANT (increased metabolic demands on the cardiac muscle fibers for continuous function. **Conduction of excitatory impulses to the cardiac sarcomeres is through - T TUBULES and SARCOPLASMIC RETICULUM
57
Name the MUSCLE - Cells joined by INTERCALATED DISKS to make a fiber - cross striations from SARCOMERE - ROUNDED NUCLEI (sometimes 2) - Has sarcomere - Connectivity organizes spread of contraction in the interconnected fibers - Exhibit AUTORHYTHMICITY (spontaneously generate stimuli) - Spontaneously generate stimuli - INVOLUNTARY
CARDIAC MUSCLE
58
How are PURKINJE fibers different from CARDIAC muscle fibers? How does purkinje fibers which can be found in cerebellum related to cardiac ?
- Thicker and larger than cardiac muscle fibers - contain greater amount of GLYCOGEN (lighter staining) - contain FEWER CONTRACTILE filaments - On either side of the interventricular septum * * Part of conduction (electrical) system of the heart * *Branch throughout the MYOCARDIUM - Deliver continuous WAVES of stimulation from the atrial nodes (SA and AV) to the rest of the heart musclulature (via gap junctions) * * stimulation produces VENTRICULAR CONTRACTIONS (systole) -ejection of blood from both ventricular chambers
59
Name the muscle - Eosinophilic cytoplasm - Minimal ENDOMYSIUM - speckled hot dog CENTRAL NUCLEUS (looks small and circular in cross section) - Fiber is a SINGLE CELL with a SINGLE NUCLEUS - NO T TUBULES - SR not well developed - ZONULA ADHERENS-binds muscle cells - Contain gap junctions - INVOLUNTARY - contain CAVEOLAE - Calmodulin - Contractile mechanism - use DESMIN and VIMENTIN - actin and myosin but NO CROSS STRIATION
SMOOTH MUSCLE
60
What is the contractile mechanism of Smooth Muscle ?
- Intermediate filament cable network of DESMIN and VIMENTIN - Dense bodies bund intermediate filaments and actin to the membrane - Actin is attached/anchored to the DENSE bodies to develop contractile force (usually actin is attached to Z line in skeletal and cardiac muscle)
61
Which Component of smooth muscle allow for rapid ionic communication btw smooth muscle fibers (coordinated activity) and provide functional coupling?
GAP JUNCTIONS
62
Which component of the SMOOTH muscle : - vesicular invaginations of the cell membrane - CONTROL influx of CALCIUM into cells following stimulation * ** same effect has T TUBULE in skeletal and cardiac muscle.
CAVEOLAE
63
Differentiate btw smooth and striated muscle (skeletal and cardiac)? Which has sarcomere? Which has actin and myosin? Which has SR/ T-Tubules? Regulation?
- Actin and myosin but NO SARCOMERE in SMOOTH MUSCLE (Actin connects to IF cytoskeleton and dense bodies - connect to SARCOLEMMA) - SR but NO T TUBULES - can be innervated but also REGULATED by ; Hormones, stretch, spread from cell to cell by GAP JUNCTIONS
64
SUMMARY TABLE OF skeletal, cardiac and smooth muscle Location of nuclei ``` *Categorize in order of Multiple nuclei (Peripheral) Central nuclei (1 or 2), central nuclei (single) ```
SKELETAL CARDIAC SMOOTH
65
SUMMARY TABLE OF skeletal, cardiac and smooth muscle Which is has SARCOMERE structure? Which does not?
Has Sarcomere SKELETAL CARDIAC No Sarcomere SMOOTH MuSCLE
66
SUMMARY TABLE OF skeletal, cardiac and smooth muscle Which HAS/NO INTERCALATED DISC
HAS INTERCALATED DISC CARDIAC MUSCLE NO Intercarlated disc Skeletal Smooth
67
SUMMARY TABLE OF skeletal, cardiac and smooth muscle What has branches?
Has BRANCHES CARDIAC MUSCLE NO branches Skeletal Smooth
68
SUMMARY TABLE OF skeletal, cardiac and smooth muscle Which has cell-cell GAP JUNCTION
GAP JUNCTIONS CARDIAC SMOOTH NO GAP Junction Skeletal
69
SUMMARY TABLE OF skeletal, cardiac and smooth muscle Which has T TUBULE
HAS T TUBULES SKELETAL CARDIAC - larger NO T tubules Smooth
70
SUMMARY TABLE OF skeletal, cardiac and smooth muscle | Has SR SARCOPLASMIc reticulum -How does it affect calcium?
ALL have SARCOPLASMIC RETICULUM, nucleus and Mito SKELETAL- yes CARDIAC- less well developed SMOOTH- less well developed **CARDIAC and SMOOTH muscles can’t sure enough CALCIUM for uninterrupted contraction due to less developed SR
71
SUMMARY TABLE OF skeletal, cardiac and smooth muscle Has mitochondria?
ALL HAVE MITOCHONDRIA, nucleus and SR MITO Skeletal muscle Cardiac - larger and MORE ABUNDANT Smooth
72
In skeletal muscle for example, the actin and myosin filaments are bound to proteins that help them bin to the Z line. What are the proteins that help ACTIN bind to Z LINE ? Whatcha help MYOSIN bind to Z LINE
A(alpha) - Actinin -Bind actin to Z line | TITIN - bind myosin to Z line
73
What is the determination/differentiation of skeletal muscle (myogenic) cells ? State the process from STEM CELL TYPE to end product
- TOTIPOTENT stem cell differentiate into 3 germ layers (Ectoderm, mesoderm and endoderm) - MESODERM stem cells can differentiate into adiboplasts, myoblasts and chondroblast - single cell MYOBLASTs can then differentiate fo form multinucleated MYOTUBE (when the extracellular conc of growth/transcription factors drop below critical threshold) **Cells that differentiate into MUSCLE no longer divide
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What determines if myoblasts cells became myogenic/skeletal muscle? Give examples?
TRANSCRIPTION FACTORS - MyoD - myogenin - myf-5 - MRF-4/Herculin/myf-6
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Describe the structure and function of myoD? WHat do the 2 regions help with? What binds proteins? What binds DNA? What is the DNA sequence called? Where is it seen most?
STRUCTURE - nuclear phosphoprotein - bHLH region (BASIC HELIX-loop-helix) FUNCTION? - HELIX (HLH) region of myoD form DIMER with E2 family proteins (*E2A - E12, E47, *E2-2,*HEB) - BASIC region of myoD BIND DNA better (10x) as heterodimer **DNA sequence called E-box (present in most MUSCLE SPECIFIC ENHANCERS in multiple copies))
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Describe the process of transcription activation in skeletal muscle physiology? How many Ebox must be bound? What will happen to the muscle genes that have no E-boxes?
- MyoD complexes must bind to 2 or more upstream E-BOXES - some muscle genes have no Ebox but are still regulated by myogenic intermediate proteins - SPECIFIC binding to activate transcription (has to be BASIC region) - MyoD initiates chromatin remodeling in regulatory regions of muscle-specific genes
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MyoD is one of the transcription factors that determines if cells become myogenic? What can cause NO activation of transcription? What region f MyoD does specificity reside in?
Binding has to be SPECIFIC to activate transcription - fusing BASIC region of MyoD to non-muscle HLH region leads to dimer via HLH, specific binding to DNA and ACTIVATION of muscle genes - if you SWITCH basic regions of proteins, you will see dimerization and binding but NO ACTIVATION ***SPECIFICITY of myogenic activation resides in the BASIC REGION
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MyoD, MRF4, Myf5 and myogenin and transcription factors that determine the role of myogenic proteins. At what stages are they determining factors?
MyoD and Myf5 - EARLY | Myogenin and MRF4- Late
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A 9 month old is brought to the hospital by his concerned parents because he can do push ups and can lift 7 lbs weights. Test show mutation in a signaling protein What protein is this? How does it affect muscle growth? What does it inhibit? How is it activated?
MYOSTATIN mutations - MYOSTATIN is a member of the TGFb family of SIGNALING proteins - It is a negative regulator of muscle growth (mutations can lead increase in muscle mass) - INHIBIT myoblast proliferation and progression from G1 to S - MyoD binds to E box in myostatin promoter and activate myostatin transcription
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How does change in myostatin affect muscle cells/mass
- Gain of function/Overexpression of myostatin lead to fewer muscle cells (Hypotrophy) - Loss o function/Underexpression of myostatin lead to increased muscle cells (hypertrophy) **Myostatin works to INHIBIT muscle growth/cells/mass
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Skeletal muscle is able to repair itself after damage by recruitment of? How? Location? Composed of?
SATELLITE CELLS - recruited to SUPPLY MYOBLASTS for repair and regeneration - located on SURFACE OF MUSCLE FIBER, beneath the basal lamina - for 2-7% of muscle nuclei in healthy individuals - normally quiescent until needed - increase muscle mass after exercise
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Skeletal muscle is able to repair itself after damage by recruitment of? How are these cells recruited? What is the normal state before need?
SATELLITE CELLS Normally quiescent until needed - process activated by IMMUNE RESPONSE to injury - satellite cells start dividing (form new muscle fibers and reconstitute pool of satellite cells) - migrate to site of injury - follow normal differentiation pathway
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What happens to muscle mass after exercise? Describe the process? How does satellite cell come into play? What regulates satellite cell activity? How?
Muscle mass INCREASES after exercise - hypertrophy of existing cells - weight training damages muscle (micro trauma) - activates satellite cells (cells start dividing and repair damage which would INCREASE the size and thickness of muscle fiber) - growth factors and hormones REGULATE satellite cell activity (increase in protein synthesis and glucose uptake) - TESTOSTERONE stimulate release of hormones - have direct regulatory effect on satellite cells
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``` Actin Myosin Tropomyosin Troponin TITIN Nebulin ``` All components of what? What happens here?
MUSCLE SARCOMERE | **Where contraction occurs
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Myosin is a component of muscle SARCOMERE. What are the 3 component of myosin What properties does myosin have and how does it relate to its function -contraction?
1) 2 heavy chains - each has a globular head (has ATPase) and a filamentous tail (alpha helical tail) 2) 2 light chains - 2 pairs- essential light chain on top, regulatory light chain below 3) Crossbridges - component of head region - project laterally from the thick filament - LINK between thick and thin myofilaments * *Has BIOLOGICAL PROPERTIES - acts as ATPase which release chemical energy for contraction - binds to actin - both properties located in GLOBULAR HEAD
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Name the component of muscle sarcomere? - lies in the groove between the two strands of actin - has a regulatory function and provides structural rigidity to ACTIN
TROPOMYOSIN
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Troponin is one of the components of muscle sarcomere. It is made up of a complex of 3 proteins. Where is TROPONIN located? Name the type of troponin - serves to bind troponin to TROPOMYOSIN - contains 2 high and 2 low affinity for CALCIUM - INHIBITS interaction btw actin and myosin
Troponin is located at the end of TROPOMYOSIN molecule - TROPONIN T - TROPONIN C - TROPONIN I
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Name the component of muscle sarcomere - one molecule extends from M line to Z disc - acts as spring to keep MYOSIN filaments centered in sarcomere and maintain resting tension that allows muscle to snap back in overextendened
TITIN
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Name the component of muscle sarcomere - associated with actin - regulated the assemble and alignment of acting filaments (keep it in place)
NEBULIN
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WHat is the role of CALCIUM in muscle contraction/relaxation?
- in relaxed muscle, level of free cytosolic CALCIUM is low - in stimulated muscle, INTRACELLULAR CALCIUM levels increase substantially - CALCIUM binds to TROPONIN C to change conformation of complex - when stimulation stops, CALCIUM levels decrease and dissociate from regulatory protein and muscle RELAXES
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Movement of what mediates the activity of muscle excitation and contraction? What are the events called?
CALCIUM **events that describe CALCIUM movements in muscle cells is called EXCITATORY-CONTRACTION COUPLING
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Process of E-C coupling
- nerve excite motor end plate to depolarize and cause AP in T-tubular system of sarcolemma - T-tubules contain VGCa channels (DHP or Dihydropyridine) that mediate long lasting Ca2+ currents -channel act as VOLTAGE SENSOR - WHen T-tubules depolarize, calcium is released from terminal cisternae of SR - calcium release from SR takes place with separate calcium channels (RYANODINE receptor 1 or RyR1) - SR Ca2+ channel comes in close proximity to DHP channel proteins in T-tubule membrane - conformation changes in DHP channels cause RyR1 channels to open through protein-protein interaction - Ca2+ are recaptured by SERCA (sarcoendoplasmic reticulum calcium ATPase) in SR and returned to terminal cisternae
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WHat is the affinity/interaction btw actin myosin and how does change in the presence/absence of other factors
MYOSIN has a VERY HIGH affinity for ACTIN and would very TIGHT bonds in ABSENCE of TROPOMYOSIN and ATP - ATP dissociate myosin-actin complex by binding to myosin - AT REST, tropomyosin lies on the outside groove btw actin chains and blocks interaction of actin and myosin - When CALCIUM enter SARCOPLASMIc and binds to Troponin C, conformational change occurs in tropomyosin - tropomyosin molecule moves and exposes active sites on actin - shift enables nearby myosin crossbridges to attach to actin active sites
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Describe the cycle of the Sliding filament model of muscle contraction 4 steps
1) cycle starts with MYOSIN tightly bound to ACTIN, When ATP binds MYOSIN, actin is released (MA)+ ATP = (M-ATP) + A 2) ATPase on the globular head of MYOSIN myofilament hydolyzes ATP to ADP and Pi **conformational change occurs and Myosin now in high energy conformational state **release of Ca2+ exposes binding site on actin and energized myosin head binds to actin 3) Pi dissociate 4) ADP dissociate * *release of Pi and THEN ADP causes myosin head to turn causing ratchet movement
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What happens after Pi and ADP dissociate in the last 2 stages of the sliding filament model of skeletal muscle What shortens the sarcomere? WHat is this called?
- The release of Pi and ADP cause myosin head to turn in ratchet movement - This translocated actin filaments toward the M line of sarcomere, pulling Z bands toward each other- This would shorten the sarcomere - POWER STROKE - contractile proteins remain tracked until another ATP molecule binds to myosin - cyclic myosin-actin interactions will continue until Ca2+ ions are removed from SARCOPLASM * *USEFUL ANALOGY/SUMMARY - ATP cocks myosin trigger - formation of actin-myosin complex pulls the trigger - energy stored in cocking the trigger is released
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In the absence of ATP in the sliding model, WHat will happen to actin and myosin? WHat is this called? What is the main source of energy in skeletal muscle contraction?
RIGOR MORTIS -dead people **ACTIN remains BOUND to MYOSIN and can’t be released -ATP CLEAVAGE - main source of energy for contraction
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Name the channel - responsible for large resting chloride conductance of skeletal muscle - stabilizes resting membrane potential preventing false action potentials - important in REPOLARIZING membrane following contraction
CHLORIDE CHANNEL (ClC-1)
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There are 3 types of contraction Name this - single A.P case release ENOUGH Ca2+ to fully initial contraction - However, Ca2+ are REMOVED from sarcoplasm so RAPIDLY that muscle cell don’t have enough time to develop maximum force
TWITCH CONTRACTION
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There are 3 types of contraction Name this How does summation contraction work and how is it different from other contraction? What will summation contraction result in?
SUMMATION contraction - absolute refractory period of motor nerve is much SHORTER than TWITCH contraction - This can enable a SECOND stimulus to be applied to muscle cell before relaxation is complete (Basicaly 2 TWICHES together) - additional Ca2+ is release to sarcoplasm before all the previously released Ca2+ is Removed by SR **RESULT in -: INCREASE in intracellular Ca2+ INCREASE in number of crossbridges formed INCREASE in amount of tension developed
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There are 3 types of contraction Name this - When rate of stimulation of motor nerve INCREASES to a point where there is LITTLE or NO relaxation evident - Level of TENSION reaches MAXIMUM PLATEAU - Continuous signal/contraction/Tension
TETANUS CONTRACTION
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Describe the process of SKELETAL MUSCLE RELAXATION
- NO more AP generated at NMJ so SARCOLEMMA returns to its RESTING electrical potential as does entire T TUBULE system and SR membrane - myosin remains in high energy conformational state but NOT BOUND to actin - sarcoplasmic calcium then pumped back into SR cisternae by extremely active ATP-driven calcium pump SERCA - Ca2+ has higher affinity for pumps than for troponin C - SR contains calsequestrin, a glycoprotein that binds Ca2+ ions and which acts to reduce SR concentration of free Ca2+
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small pool of ATP present in muscle but is continually replenished by ? - what catalyze the phosphorylation of ADP to ATP? WHat does it use? - What is metabolized in muscle during contraction to provide what to use to generate ATP? Via what 2 mechanisms? WHat are the 3 sources to generate ATP? Which is most ABUNDANt?
-CREATINE PHOSPHATE - CREATINE PHOSHOKINASE using creatine phosphate * *first source used to generate ATP -GLYCOGEN in muscle provide GLUCOSE **Via GLYCOSIS (second source to generate ATP) and OX.PHOS (third and MOST ABUNDANT source of ATP)
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Which basic type of contraction is this: - Muscle DECREASES in length against opposing load, such as lifting weight up - keep a constant tension - muscle contracts, shortens and creates enough force to move the load
CONCENTRIC ISOTONIC contraction
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Which basic type of contraction is this: - Muscle INCREASES in length as it resists load, such as pushing something down - muscle contracts, SHORTENS and creates enough force to move load
ECCENTRIC ISOTONIC contraction
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Which basic type of contraction is this? - muscle does NOT SHORTEN - Tension builds up - Force CANNOT move load WHat are most real contractions?
ISOMETRIC CONTRACTION ***Most real contractions are mixtures of ISOTONIC AND ISOMETRIC contractions
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What is the relationship called you can: - vary amount of active tension of muscle cell by changing its length - can measure different types of tension (ISOMETRIC) generated by changing length of muscle **When is Optimal length (Lo) reached?
LENGTH-TENSION relationship **Lo- length of muscle where maximum force is generated and most crossbridges formed (point B on graph)
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There are 3 points on the length-tension relationship graph, what 3 things happens at point C?(Descending)
- muscle is STRETCHED too far that actin and myosin hardly overlap - FEW cross-bridges - LITTLE tension
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There are 3 points on the length-tension relationship graph, what things happens at point B?
- many ACTIVE cross-bridges - isometric TENSION will be HIGH - OPTIMAL LENGTH (Lo)
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There are 3 points on the length-tension relationship graph, what things happens at point A? (Ascending)
- a lot of overlap of actin and myosin | - actin filaments lush on each other distorting filaments and WEAKEN crossbridges
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Name the type of tension - generated by STRECHING muscle to different lengths - also called PRELOAD - caused by resistance of muscle’s elasticity to stretch - NOT caused by actin-myosin crossbridges
PASSIVE TENSION
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Name the type of tension -generated when muscle is stimulated to contract at different preloads
TOTAL TENSION ** sum of tension generated by crossbridge formation and passive tension
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Name the type of tension -generated by contractile process (actin-myosin crossbridges)
ACTIVE TENSION **Calculated by subtracting passive tension from total tension
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What type of relationship is established by holding LOAD on muscle CONSTANT and measuring rate of change in muscle length? **What type of contraction is this similar to?
FORCE-VELOCITY or LOAD-VELOCITY relationship **ISOTONIC CONTRACTION
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In force-velocity relationship, shortening (DECREASE) velocity is determined by? (3) *Factors that determine the velocity of contraction
- INCREASE load on muscle (after load) - number of active crossbridges - rate of crossbridge cycling
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There are 3 factors that determine the velocity of contraction? How does LOAD affect velocity?
- No load =maximum velocity (Vo or Vmax) - INCREASE in load causes DECREASE in velocity. - load on muscle is called AFTERLOAD
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There are 3 factors that affect velocity of contraction. How does Number of active crossbridges affect velocity?
-MORE cross bridges actively contribute to shortening contraction, lead to GREATER the contraction velocity at ANY given LOAD
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There are 3 factors that affect velocity of contraction. How does rate of crossbridge cycling affect velocity?
- entire process largely dependent on type of myosin ATPase, fast or slow - skeletal muscle cells either have fast or slow myosin ATPase - different types of fibers depending on ATPase type - each muscle has only one type of myosin ATPase, but ALL muscles have a MIXTURE of fast and slo fibers
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Name the fiber type: - slow myosin ATPase - loaded with MITOCHONDRIA - depend on CELLULAR RESPIRATION for ATP production - RICH in myoglobin, hence RED in color - HIGH RESISTANCE to fatigue - activated by SMALL, SLOW-CONDUCTING neurons - used for activities with repeated low-level contraction e.g MARATHON, maintaining posture
Type I fibers **known as “slow-twitch” fibers
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Name the fiber type -fast myosin ATPase
TYPE II FIBERS * *known as “fast-twitch fibers - further divided into IIa and IIb
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Name the fiber type - loaded with MITOCHONDRIA - depend on CELLULAR RESPIRATION and GLYCOLYSIS - RICH in myoglobin, RED in color - MODERATE Fatigue-resistant - activated by LARGE, FAST-CONDUCTING motor neurons - used for activities involving speed, strength and power e.g sprinting, walking
TYPE IIa FIBER **Fast oxidative stress
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Name the fiber type - FEW mitochondria - RICH in GLYCOGEN - depend on GLYCOLYSIS - LOW in MYOGLOBIN, WHITISH in color - FATIGUE easily - activated by LARGE, FAST-CONDUCTING motor neurons - used for activities requiring short, fast bursts of power e,g hitting a baseball
TYPE IIb FIBERS ***Fast Glycolytic Fibers
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Normal skeletal muscle contraction always involves groups of muscle cells. What is the group of muscle fibers innervated by same motor neuron called?
MOTOR UNIT * *AP from a single neuron will call all muscle fibers of that motor unit to contract simultaneously * *Number of fibers innervated by motor unit is called INNERVATION RATION
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Different types of motor units innervate different types of muscle fibers Name the motor unit: - small diameter - few muscle fibers innervated- small interaction ratio - slower conducting - lead to FINE GRADED movements
TYPE I MOTOR UNITS **Innervate type I muscle fibers
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Different types of motor units innervate different types of muscle fibers Name the motor unit: - more muscle fibers innervated - LARGE innervation RATIO - faster-conducting - lead to COARSE movements
TYPE II MOTOR UNITS **Innervate type II muscle fibers
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TENSION can be increased in entire muscle in which 2 ways ?
1) RECRUITMENT -increasing number motor unites (i.e muscle fibers) contracting - recruit first slow-twitch (type I), fast twitch (type IIa then IIb) 2) SUMMATION - increasing FREQUENCY of individual motor unit firing
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What is this :- - decline in ability of muscle cells to generate force - intracellular glycogen and creatine phosphate stores depleted - ATP levels do not decrease substantially - lactic acid buildup
MUSCLE FATIGUE **lactic acid buildup is NOT due to muscle fatigue
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What occurs in muscle with aging ?
1) ATROPHY - DECREASE muscle mass and strength called SARCOPENIA/DISUSE (fewer satellite cells) - Decrease total number of fibers, maximum force and power of contraction - DECREASE in number of mitochondria 2) MOTOR UNITS - DECREASE in motor units - INCREASE in number of fibers per motor unit * *MEN loose muscle mass FASTER than women * *Weight/strength training help reduce the amount of muscle mass lost with age
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Name the muscle disease - progressive skeletal muscle weakness, defects in muscle proteins and death of muscle cells and tissue - mutations in gene - Mutations lead to instability of sarcolemma - This instability leads to DAMAGE of muscle during contractions What gene/protein is mutated
MUSCULAR DYSTROPHY **2 forms - Duchenne (from 3 years old) and Becker (from teens- milder) -MUTATIONS in DYSTROPHIN gene
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Name the muscle disease - PRIMARY SYMPTOM is muscle weakness. Others are; muscle cramps, stiffness and spasms - prognosis varies from stable with little or no disability to progressive, severely disabling, life-threatening or fatal What are the 3 causes?
MYOPATHIES Causes - congenital - genetic abnormalities in mitochondria - mutations in genes controlling enzymes that metabolize glycogen and glucose
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Name the muscle disease - aka “wasting syndrome” - loss of weight, muscle atrophy, fatigue, weakness, loss of appetite - seen in patients with CHRONIC diseases such as cancer, AIDS, diabetes, multiple sclerosis, congestive heart failure -similar to what?
CACHEXIA **similar to sarcopenia/disuse/loss of muscle mass
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Name the muscle disease - INFLAMMATION of muscles - results in muscle weakness and pain, particularly in muscles closes to TRUNK - caused by injury, infection or autoimmune disease
MYOSITIS
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Name the muscle disease - breakdown of muscle fibers resulting in release of muscle fiber contents (MYOGLOBIN) into the circulation - some of these are TOXIC to the kidney and frequently result in KIDNEY DAMAGE - MOST common CAUSES - crush injury, overexertion, alcohol abuse, certain drugs (STATINS), toxic substances
RHABDOMYOLYSIS
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Name the muscle disease - defects is RYR1 channel - cause channel to open more easily and close more slowly - activated by certain ANESTHETICS (halothan, isoflurane) and muscle relaxers (succinylcholine) given during surgery - leads to uncontrolled release of Ca2+ - muscle contract abnormally, leading to rigidity and heat production
MALIGNANT HYPERTHERMIA
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WHy do sensory systems exist?
- To monitor the external and internal environment so that organism can make adaptive changes in behavior - To regulate behavior, sensory systems interact with motor systems on multiple levels
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There are 3 steps involved in sensation Which 2 are essential for every sensory function? Which 1 is not essential for every sensory function
Essential for all ; TRANSDUCTION ENCODING Not essential for all ; PERCEPTION
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Which step of sensation respectively: - representation of qualitative and quantitative aspects of the stimulus - conversion of physical signal (energy) into neural signal (change in membrane potential) - Conscious awareness of stimulus
- ENCODING - SIGNAL TRANSDUCTION - PERCEPTION * *perceprions is not necessary for all because something like change in BP can not be sensed consciously yet N.S can sense it and make necessary compensatory changes
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Each sensory system extracts information about 4 basic stimulus attributes: WHich is which: -QUALITY of stimulus (determined by nature of energy transducer by the sensory receptor type) -STRENGTH of the stimulus -LENGTH of the stimulus -SITE of the stimulation
- MODALITY * *there are 5 sensory modalities- touch (somatosensation), taste (gestation), smell (olfaction), hearing (audition) and sight (vision) - INTENSITY - DURATION (SLOWLY adapting receptors provide info on duration) - LOCATION (depends on sensory receptive field and central processing)
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What is the unique form of energy that activates a specific receptor at lowest energy level WHAT attribute of stimulus is this?
ADEQUATE STIMULUS E.g light is the adequate stimulus for photoreceptors -Modality
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What is the lowest intensity which can reliably be detected 50% of the time? What is this related to ? What stimulus attribute?
SENSORY THRESHOLD -inversely related to sensitivity Threshold = 1/sensitivity **decrease in sensitivity increase the threshold and shift the intensity-response curve to the RIGHT - INTENSITY - Threshold is NOT FIXED. It is influenced by; practice, fatigue, stress, context, spectating etc.
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Receptor output DO NOT match stimulus duration due to what ? What stimulus attribute? What are the 2 types of receptors?
ADAPTATION- a decrease in receptor output despite constant sensory input -Duration * 2 Types of adapting receptor 1) SLOWLY adapting receptor- provide info about static properties of stimulus (DURATION of stimulus) 2) RAPIDLY adapting receptors - provide info about the dynamic aspects of a stimulus (change in stimulus INTENSITY)
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What is the specific spatial location within the sensory organ where stimulus energy is effective ? What stimulus attribute?
RECEPTIVE FIELD * FOr tactile receptors, the receptive field is a specific topographic location on the skin * At higher levels in a sensory system (brain and spinal cord), info from sensory receptors may be combined to alter the way sensory location is perceived -Location
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Somatosensory functions is in 2 ways of sensory transduction - What are the 2? Explain them
1) Mechanotransduction -mechanical stimulation (pressure, vibration, stretching of skin) activates mechanically gated/stretch-activated, non-selective cation channels (permeable to NA+ and K+) in the receptor cell membrane -for some mechanoreceptors, transmission of physical stimulus (energy) to the cell membrane is modulated by external, accessory structure associated with the receptor E.g pacinian and meissner corpuscles and muscle spindles 2) Temperature (hot/cod) sensory transduction - transduction of hot/cold stimuli into neuronal activity involves some members of a large and diverse family of ion channels called TRP channels (Transient Receptor Potential). Permeable to mono and divalent cations
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How does TRP channels transducer hot/cod stimuli into neuronal activity? How do you activate the TRP channels ? What are the different cutaneous receptors
- TRP channels are VARIABLY permeable to mono and divalent cation channels depending on the specific TRP channel type - some channels activated by cold/warm temperature - some may also be chemically gated (both temperature and protons cause channel to open) - Temperature sensitive TRP gated within specific temperature changes - CUTANEOUS receptors contain temp sensitive TRP channels and can act as cold or warm receptors Receptors * *Cold (12-36C) - stimulated by LOW temp and MENTHOL (compound isolated form mint that produce a cool sensation when applied to temp sensitive areas) * *Warm (30-47C) -stimulated by HIGH temperatures and CAPSAICIN (vallinoid compund - isolated form hot chili peppers)- produce sensation of heat wen applied to temp sensitive areas * *Termal pain/nociceptors - activated by EXTREME of heat or cold. less that 12C or more than 47C
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In ENCODING, the opening of mechanically r thermally gated channels results in a receptor potential analogous to a conductance increase EPSP. Describe which stimulation in the following scenarios: - Receptor potential DOES NOT depolarize axon initial segment to threshold there AP NOT FIRED - Receptor or generator potential DOES depolarize axon initial segment above threshold, triggering AP
- Subthreshold stimulation | - Suprathreshold stimulation
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The intensity of stimulations is encoded by the frequency of action potential firing. What is this called?
FREQUENCY CODING * *A weak stimulus, barely sufficient to depolarize the receptor cell to threshold results in a low rate of AP firing * *A strong stimulus produces a large receptor potential, causing rapid AP firing
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Adaptation - REDUCED output despite CONSTANT stimulation- can result from what 2 mechanisms ?
1) Sensory mechanisms - the sensory transduction processes itself may adapt, This occurs through physical changes in capsule in pacinian and meissner corpuscles 2) Membrane mechanisms - membrane process/ion channel gating also cause adaptation - Ca2+ activated K+ channels - variety of potassium channel gated by intracellular or cytoplasmic calcium
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Explain the process of Ca2+ activated K+ channels Where are VGCa2+ channels found ? What is the result?
-Voltage gated Ca2+ channels are PRESENt in the presynaptic active zone and also in areas of neuron membrane that integrate input signals (receptor potentials for sensory neurons and synaptic potential for central neurons) - VGCa2+ channels open briefly during each AP. - During repeated high frequency firing, Ca2+ gradually accumulated in the cytoplasm which will - eventually activate Ca2+ depending K+channels **The additional K+ conductance cause the membrane potential to sag back towards the resting level, reducing the rate of AP firing
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Classification of somatosensory receptors is based on what properties?
1) Anatomical - Encapsulated sensory endings - Non encapsulated sensory endings 2) Functional - Adaptation - Threshold - Conduction velocity
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Which receptors include free nerve endings, merely endings and hair follicle receptors?
Nonencapsulated cutaneous receptors
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What somatosensory receptor is described? - formed by fine branches of sensory axons (MYeliNATED and UNMYELINATED) - endings lose any myelin wrappings before terminating (terminations DO NOT CONTACT specialized structures) - found throughout the body including skin, joints and viscera - all have similar structures but different function as mechanical, thermal, pain or itch receptors depending on the sensory transduction mechanisms present in the nerve ending
Free nerve endings (Non-encapsulated receptors) **fast or slow adaptation rates
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What somatosensory receptor is described? - formed by MYELINATED axons of sensory receptor neurons that branch into FLAT, DISK-SHAPE endings. - Endings CONTACT specialized specialized cells in the basal layer of the epidermis - contain stretch-gated ion channel and function as MECHANORECEPTORS - cells contacted by the endings CONTAIN VESICLES, and the point of contact resembles a synapse
MERKEL ENDINGS (Non-encapsulated) **Recent findings indicate merkel cells with stretch-gated channels are important contributors to the TACTILE response properties of the merkel sensory neurons
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Name the somatosensory receptors - MECHANOREcEPTOrs formed by endings of sensory axons (THIN MYELINATED) - rapidly adapting
HAIR RECEPTOR REcePTORS (Non-encapsulated) - wrap around hair - Bending of the hair stretches the axon membrane, OPENing stretch-gated channels and produce firing - stop firing when the bent position is held
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Name the somatosensory receptor - ALL are MECHANORECEPTORS with stretch-gated ion channels - All have MYELINATED axons
ENCAPSULATED RECEPTORS * Pressure applied to the skin is transmitted through the capsule to the axon endings within the capsule * The mechanical properties of the capsule alter the transmission of pressure to the sensory endings thereby altering their response properties
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Name the somatosensory receptors - contain a LAYERED stack of SCHWANN CELLS within a capsule - The Schwann cells are oriented perpendicularly to the long axis of the capsule - One or more axon endings wind btw the Schwann cell layers - Meissner corpuscles are located just under the epidermis of HAIRLESS/glabrous skin
Meissner corpuscles (Encapsulated receptors)
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Name the somatosensory receptors - subcutaneous - caspsule contains CONCENTRIC layers of EPITHELIAL cells with FLUID filled spaces between - A single axon ending lies in the center of the corpuscle
Pacinian corpuscles (Encapsulated) -squishy onion appearance
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Name the. Somatosensory receptors - located in the DERMIS and in subcutaneous and connective tissue - The capsule contains a core of longitudinally oriented COLLAGEN strands with INTERSPERSED sensory endings - response to DRAG or SEARING forces that apply tension to the collagen strands, squeezing the axon endings that pass between the strands
Ruffini endings (Encapsulated receptors)
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What is the classification based on the pattern of AP generation during steady, sustained sensory stimulation?
Somatosensory receptors classified as RA or SA * RA-rapidly adapting (encapsulated pacinian, meissner, hair follicle receptors * SA-slowly adapting (Mekel and Ruffini receptors) **Free nerve endings have either slow or rapid adapting rates
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- Which receptor respond when pressure is applied or released?? (I.e when pressure changes rapidly, most sensitive to FAST VIBRATIONS) - Which lose their normal rapid adaptation and respond to sustained firing during constant sensory stimulation - Which is “tuned” to respond to LOWER frequencies of vibration?
- Encapsulated pacinian corpuscles - Decapsulated pacinian corpuscles - Meissner corpuscles
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There are 3 functional classifications of somatosensory receptors : adaptation, threshold and conduction velocity. How is threshold classified? Depending on what?
- Classified as high or low threshols based on SENSITIVITY or sensory stimulation - High threshold have low sensitivity and require GREATER stimulation (e.g free nerve endings that function as mechanoreceptors) - Low threshold have high sensitivity and require less stimulation (e.g meissner, pacinian, merkel and ruffini)
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WHat are the receptors found on hairy vs hairless skin?
Hairy - Hair follicle receptors - Merkel and Ruffini - Free nerve endings - Pacinian corpuscles (deeper tissue layers) Hairless - Meissner receptors - NO hair follicle receptors (HAIRLESS DUH!!!)
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What is the specific spatial location where a stimulus is effective at activating a single receptor cell How do these vary?
Receptive field ** Receptive field size varies with receptor type and with body location SMALLEST - digits of hands (finger tips cheek,close, upper limb) , LARGEST - trunk and limbs (thing,calf,shoulder,back)
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How does receptive fields relate to resolution?
* *HIGH receptive fields - LOW spatial resolution - touch anywhere it will fire but DON’T KNOW SPECIFIC point touch - e.g Pacinian and ruffini corpuscles **LOW receptive fields - HIGH spatial resolution E.g Meissner and Merkel receptors - tested by minimum spacing required to detect 2 test points (2-point threshold) - 2 stimuli simultaneously applied closer than the threshold range will be perceived as a single stimulus
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Relate the response properties (adaptation, threshold, distribution and receptive field to the specific sensory functions of somatosensory receptors 1) Pacinian -Ab (Large myelinated) 2) merkel - Ab (Large myelinated) 3) Meissner- Ab (Large myelinated) 4) Ruffini - 5) Free nerve ending - Ad and C-fiber 6) Hair follicle receptors - Ad thin myelinated
1) respond to FAST VIBRATIONS or changes in pressure. Respond to change in pressure when object is first grasped in hand (EVENT DETECTORS) Fast adapting, high receptive field, low spatial resolution and sensitivity , higher threshold than meissner 2) signal the weight, form and surface features of objects contacting the skin. Slow adapting (sustained response) allows them to signal the STEADY PrESSURE exerted by the edges of the objects held in the hand (STATIC properties, DURATION) 3) MOST abundant in the HAND. RAPID adaptation, DO NOT provide info about static properties however they readily DETECT textures and edges as the hand is moved over surfaces. Merkel and Meissner- low receptive field, HIGH spatial and temporal resolution (READING BRAILLE TEXT) 4) respond to STRETCH of skin (have collagen) signaling POSTURE and MOVEMENTS of the body including the hand and mouth (slow adapting, high receptive field, low spatial resolution) 5) DIVERSE function. Nociceptors (extreme temp), Mechanoreceptors (high threshold, low sensitivity- CRUDE TOUCH SENSATION), Thermal receptors (TRP channels -cold/warm), itch respecters (chemical: histamine) THIN UNMYELINATED AND MYELINATED 6) respond while hairs are being bent, allow sensation of air objects and nearby object that have not touched skin (fast adapting) THIN MYELINATED
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What are the receptors found in the muscle and joints? (5) and functions?
1) MUSCLE SPINDLES - provide sensory information about muscle LENGTH, and receptor type activated by TENDON TAP to elicit STRETCH REFLEX 2) GOLGI TENDON ORGANS - provide info about Muscle TENSION - can also contain free never endings that provide PAIN sensory info in response to muscle INJURY/over use 3) FREE NERVE ENDINGS - mediate joint pain 4) RUFFINI ENDINGS - some info about joint MOVEMENTS that cause stretching of the skin 5) PACINIAN CORPUSCLES - near PERIOSTEUM - provide info about bone VIBRATIONS
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How are myelination status, axon diameter and conduction velocity used to differentiate sensory fibers in peripheral nerves ? * *Match the type and function 1) Largest axon diameter, Myelinated, highest conduction velocity (70-120m/s) 2) 2nd largest axon diameter, Myelinated, 2nd fastest conduction velocity (35-70) 3) 3rd largest/moderate axon diameter, Myelinated, conduction velocity (10-40) 4) 4th axon diameter, Thin Myelinated, velocity (5-35) 5) 5th small axon diameter, Myelinated, low velocity (3-12) 6) smallest axon diameter, UNMYELINATED, lowest velocity (0.5-2)
1) Aa - muscle spindle primary afferent (Ia) - a-motor neurons - Golgi tendon organs (Ib) 2) Ab -(II), - cutaneous touch and pressure, - muscle spindle secondary afferent 3) Ay - y-motor neurons 4) Ad (III) - hair follicle receptors - fast nociceptors - thermal and crude touch receptors 5) B fibers - preganglionic autonomic 6) C fibers - postganglionic autonomic - slow (polymodal) nociceptors that respond to mechanical, thermal and chemical stimulation - itch receptors
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Fast and slow pan relative to differences in peripheral nerves
Fast pain - Fast nociceptors (Ad fibers) - mechanical and thermal stimulation - sharp,pricking and localized Slow pain - nociceptors with small, unmyelinated axons (C fibers) - delay compared with fast pain. - subjective qualities (aching, throbbing, burning) * *Time difference btw fast and slow is explained by differences in conduction velocity * *Perceptual differences explained by differences in CNS pathway and sensory processing
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WHich is which - Bathing, dressings, feeding, hygiene, transferring, toileting * *”Have to be able to do these before you can go to SCHOOL” - Shopping, housework, taking prescribed medications, managing money, using the telephone and other technology, transportation * * Have to be able to do these before going to COLLEGE
- Activities of daily living (ADL) | - instrumental activities of daily living (iADL)
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Common changes that occurs with aging
1) body composition 2) frailty 3) cognitive changes (combative/behavior change FIRST REASON people in nursing homes 4) Vision and hearing decline (sensory deprivation) 5) falls 6) Sleep changes (less REM/deep sleep) 7) Urinary incontinence (2nd reason people in nursing school) 8) Polypharmacy 9) Vertigo 10) Syncope
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How does body composition change with aging?
- MORE brittle bones - INCREASE body fat esp around abdominal organs - DECREASED lean muscle mass - DECREASED subcutaneous fat (chance of hypothermia) - Decreased total body water - decreased protein in blood (most medication are bound to protein)
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Frailty and aging What does increased frailty ultimately lead to?
- Vulnerability in older adults due to impaired homeostatic mechanisms - Impaired immunological, cardiac, pulmonary ad renal reserves - INCREASED SNS tone - increased cortisol -IMPAIRED immune system - decreased neuroendocrine function can lead to WEAKNESS in muscles and bones - Decreased oral intake may lead to further weakness - Brain becomes more sensitive to effects of medications (less is more) **INCREASED frailty leads to an INCREASED risk of MORTALITY
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WHen are congnitive changes normal/abnormal with aging?
NORMAL DECLINE - motor speed and response times decrease - SPEED OF RETRIEVAL decreases - REMEMBERING NAMES decreases ABNORMAL DECLINE - DEMENTIA ;major Neurocognitive disorder - significant deficits in 2 or MORE areas of cognition (memory, abstract thinking, judgement, language, visuospatial functioning) - DEFICITS have to be SEVERE enough to affect normal day/day functioning
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Dementia Epidemiology/Diagnosis/Treatment Types (3) Most common
EPIDEMIOLOGY/Dx - 1/2-2/3 secondary to ALZHEIMER’s disease - VASCULAR dementia - 2nd most common dementia (white matter disease, from a big stroke that damage half of the brain) - LEWY BODY dementia - next common in autopsy studies but still controversial) **Many have mixed etiology Other causes: Hypothyroid, low Vit b12, Parkinson’s, fronto-temporal, Head injury (concussions)
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Name the dementia type 80 y.o comes in with steady decline in cognition over several years, language, naming and memory deficits with occasional VH
ALZHEIMER’s dementia
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Name the disease 70y.o comes in with frequent VH, change in LOC, frequent falls and Parkinsonism
LEWY BODY DEMENTIA
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Name the disease 45 y.o man comes in with history of ischemic stroke. Either multi-infant or small vessel “Binswangers disease”
VASCULAR DEMENTIA
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How to tx Dementia
- Proper support system for the patient - ACETYLCHLINESTERASE Inhibitors- reduce rate of cognitive decline - work close with family - PREVENT DELIRIUM - Tx psychiatric s&s of dementia (physchosis, depression, behavioral disturbance) **Congitive and behavioral changes from DEMENTIA is number 1 reason people end up in NURSING HOME
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1) How many nursing home residents/ community dwelling elderly fall? 2) Fall cause what (2) 3) difficulty in (2) 5) causes of falls
1) 1/2 nursing home residents and 1/3 community dwelling elderly fall 2) Hip fractures and head injuries 3) Difficulty in ADLs and iADLs **Lead to nursing home placements or disability 5) Neuro problems, cardio (syncope, cardia failure), medical illness (infection/UTI, DELIRIUM), environment, MEDICATIONS - -sedating meds- benzo, narcotics, barbiturates, anticonvulsant, sleeping pills -ANTICHOLINERGIC -BENADRYL (diphenhydramine), antihistamines, UTI meds) -Anticonvulsants/lithium at toxic dosage POLYPHARMACY
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Sleep changes in elderly What happens to Sleep latency Sleep fragmentation REM sleep
INCREASED sleep latency INCREASED sleep fragmentation DECREASED REM SLeep
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How does Polypharmacy affect elders
- Increased risk of sedation, cognitive changes, incontinence and falls - Dues to Decline in reserve, elders more sensitive to effects of sedating meds and drugs that interfere with Ach (ANTICHOLINERGICS- benzo, opioids, BENADRYL)
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When should depression be treated
2-3 months after incident/loss
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Most common mental illness in older adults ** most common cause of confusion and physicists in elderly
``` Anxiety disorders (most prevalent ) Cognitive impairment ``` **DELIRIUM -Common causes: hypotension, hypoxemia, infection (UTI), metabolic disarray, polypharmacy, anticholinergics/narcotics/benzos. -Although anyone can get delirious, risk factors include older age, dementia, brain damage
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Changes in the way we die
- More deaths in the hospital - More death due to chronic illness - High expectation for modern medicine to save lives - Keep expectations REALISTIC with some optimism
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How to talk about death, grief with patients and families
- Keep info OBJECTIVE with no attached EMOTIONAL labels to info - give info in SHORT and understandable bits - Take time to answer questions - if LARGE FAMILY, have ONE point of contact
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How to evaluate capacity for medical decisions
-Make sure you have stated what you are evaluating capacity for ie: Capacity to refuse potentially life saving surgery vs global ability to manage medical decisions - EVALUATE patient’s COGNITION, - May be helpful to get OUTSIDE INFORMANTS regarding recent cognitive abilities - FREE OF COERCION from family, friends or providers
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is a legal document in which a person specifies what ACTIONS should be taken for their health if they are no longer able to make decisions for themselves because of illness or incapacity. May simply appoint a decision maker.
``` ADVANCE health care directive Living will Personal directive Advance directive Advance decision ``` **Different names
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The patient, while HAVING CAPACITY, makes a decision who | will make medical, legal and financial decisions for them
Power of Attorney **BEGINS when pt NO longer have capacity or when legally directed
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Patient DOES NOT pick their medical decision maker, it is appointed by COURT ORDER, often adversarial process
Power of GUARDIANSHIP
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WHat is the correct order of who makes the substituted medical decision if not named in POA
Correct is: Spouse, Adult Child, Parent, Adult Sibling
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Kubler-Ross stages of grief
``` Denial Anger Bargaining Depression Acceptance ``` **can occur in order but are not required and do not define normal grief
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Konigsburg Concept of Grief
- Experience of grief depends on the individual temperament, life experiences and individual circumstances - Too many variables to predict reaction to grief - Human are wired to deal with grieve and don’t end assistance - There is not right or wrong way to grief
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Difference btw Grief and Depression
-both may have sadnesss, tearfulness, sleep and appetite disturbances, anxiety, decreased enjoyment -NORMAL GRIEF DOES NOT have Suicidal ideation, change in self attitude, hallucinations/delusions, total inability to function
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Action potential is generated by VG cation currents across the cell membrane. The flow of charge from extracellular to intracellular space also cause a TRANSIENT change in charge distribution btw diff points in extracellular space. How is this change in charge distribution measured?
- Measured by 2 electrodes placed in the extracellular space : 1) recording/extracellular electrode :- site of inward Na+ current flow * *Positive electrical charge is depleted at the extracellular site where inward Na+ current flows. * *This loss of positive charge is detected as a negative potential difference btw the extracellular and indifferent electrodes. * *Once AP is complete, the charge will redistribute. NO MORE NEGATIVE potential difference 2) reference/indifferent electrode :- at some distance away
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The measured AMPLITUDE of a single cell AP depends on what factors?
1) distance btw the extracellular recording electrode and the site where the membrane current flows 2) The magnitude of current flow across the cell membrane 3) The resistance of the extracellular space
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Extracellular single unit action potentials can be measured by an electrode, such as fine wire needle, inserted into a nerve so that it is close to the site of membrane current flow. - What can be done with a small unit action potential ? - Can this small unit action potential be measured? How?
- When single unit action potentials are quite small, a much LARGE potential (CAP) can be generated if MANY individual axons fire at essentially the SAME TIME (to fire simultaneously, stimulate peripheral nerve by passing electrical current through a pair of stimulating electrodes- anode to cathode) - A recording electrode placed OUTSIDE a nerve MAY NOT be able to measure the small single unit AP, but the SUM of many extracellular potentials CAP- MAY be LARGE enough to be measured with a recording electrode OUTSIDE the nerve or on the surface of skin.
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- What is the amount of stimulus current required to excite an AP in a single axon called? - How does it VARY with axon diameter? * *How is this interpreted in clinical tests of axon function?
- CURRENT THRESHOLD - Stronger stimulation/ extracellular currents for depolarization of small diameter axon (Ad and C-fibers). SMall diameter axon have higher resistance to current flow than larger diameter (Ab,Aa) - Less stimulation/ current flow will depolarize larger axon diameter due to decreased axial resistance * *Clinically, you can interpret as: - CAP evoked at low current threshold reflect function in large diameter (myelinated axons (e.g nociceptors sensory afferent, motor efferents) - High current levels needed for small diameter - current stimulation perceived as painful (slow polymodal nociceptors)
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In clinical testing of peripheral nerve function, how do you record nerve CAP? How is muscle CAP generated?
- CAP travels in either antidromic or orthodromic direction - Extracellular electrode are used to directly record the nerve CAP traveling in either direction - Easiest to record form the muscle innervated by the nerve (either motor nerve or sensory nerve -finger tips) * sensory nerve usually in ANTIDROMIC DIRECTION * *Muscle CAP generated by motor nerve conduct AP that release Ach at neurotransmitter junctions which in turn excites the skeletal muscle fibers creating a muscle CAP. * Same mechanism as nerve CAP
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The shape of Compound action potential can be either what or what depending on what?
-CAP shape is either monophasic or diphasic depending on the POSITIONS of the recording and reference/indifferent electrode. * *MONOPHASIC CAP - recorded if the reference/indifferent electrode is located AWAY from the extracellular/recording electrode site along the nerve * *DIPHASIC CAP - recorded if the reference electrode and recording electrode is NEARBY along the same nerve
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How are the negative and positive potentials shown for membrane/intracellular potentials versus extracellular potentials?
1) FOr membrane/intracellular potentials- Negative potential down and positive potential up 2) For extracellular potentials : OFTEN positive potential down and negative potential up. **OFTEN shown with this INVERTED POLARITY E.g nerve CAP, muscle CAP
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How will amplitude change in axon membrane AP versus nerve CAP?
* *AP across axon membrane : - ALL or NONE quality - AP generated with have the SAME PEAK AMPLITUDE Nerve CAP -generated by summed activity of many individual axons so amplitude will VARY depending on NUMBER of axons firing
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How does CAP latency change in unmyelinated small versus myelinated large axons
LARGE MYELINATED Axon -low intensity stimulus/ low stimulus current excites the large diameter axons, FASTEST conduction velocities, SHORT LATENCY - Conducted AP by the axons reach the recording electrode quickly SMALL MYELINATED -INCREASE in current/stimulus to excite the axons, HIGHER CURRENT THRESHOLD, SLOWER conduction velocity, LONGER LATENCY SMALL UNMYELINATED - Progressive increase in strength of the stimulation (VERY HIGH LEVELS to excite small unmyelinated C-fibers) - SLOWEST conduction velocity, LONGEST LATENCY
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When a stimulus current is delivered in the peripheral nerve twice at a short interval, the ability of axons in the nerve to fire in response to second stimuli depends on ABSOLUTE and RELATIVE refractory states of individual axons. **Differentiate btw what would happen is the second stimulus falls within either absolute or relative refractory
* *If second stimulus falls within ABSOLUTE refractory period:- 1) NONE of the axons will be able to FIRE 2) second stimulus will completely fail to evoke a CAP * *if S2 fails within RELATIVE refractory period:- 1) SOME of the axons in nerve may be able to fire - Early in relative refractory - STRONGLY hyperpolarized- few axons will be depolarized - SMALLER AMPLITUDE - Later in relative refractory - Less Hyperpolarized - more axons depolarized - At end of relative refractory- CAP of S2 will have SAME AMPLITUDE as S2
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When peripheral nerves are stimulated with strong/Supra-threshold current, the ANTIDROMIC AP reach cell bodies and 2% of the time the AP stimulate a second AP which travels in the ORTHODROMIC direction back to the muscle *What does this cause?
-Cause SMALL and VARIABLE activation of some muscle fiber called F WAVES (small, long latency, test function of proximal nerve) **M wave is normal muscle CAP (large, short latency, text function of distal nerve) **Evoking F wave is useful to test the entries motor axon function including the spinal root and peripheral nerve
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Measuring PERIPHERAL versus CENTRAL conduction velocity. | Which is which ?
CENTRAL 1) stimulate peripheral sensory fibers 2) Measure evoked responses along sensory pathway - somatosensory evoked potential - spinal cord: CORTEX LATENCY DIFFERENCE reflects central conduction velocity 3) Controlled NATURAL SENSORY STIMULATION -Visual and auditory evoked potentials are also commonly used PERIPHERAL 1) stimulate nerve at location S1 (distal) and S2 (proximal) - measure distance btw S2 and S1 2) Measure conduction time btw S2 and S1 - S2-S1 latency difference 3) Conduction velocity = distance(m)/conduction time/latency difference(S2-S1)(sec)
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Nav channel family : peripheral and central axons -VG Na+ channels formed from alpha and beta subunits What do the subunits form
Alpha subunit - LARGE forms pore of channel, contains voltage sensor, ball and chain (responsible for ESSENTIAL elements of channel FUNCTION) Beta subunit - SMALLER, modulates channel alpha subunit function (modify voltage threshold for gating and speed btw closure, activation and inactivation) * **DIFFERENT Subunit expression patterns vary by tissue/organ * **Mutations (channeopathies) affect specific tissues, DO NOT AFFECT sodium channel function THROUGHOUT THE BODY CNS channelopthy - seizures PNS channelopathy - disorder of somatosensory/pain sensation
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WHat is common cause of peripheral nerve injury What other disease of PNS? How do you dx PNS disease
DIABETES Other- GBS Guillian barre syndrome Dx peripheral nerve disease: - mutated key proteins affecting axon and myelin can disrupt peripheral nerve function - In demyelinating disease like GBS: DECREASED conduction velocity, INCREASED latency of CAP - In disease that damage AXON: DECREASED amplitude, NO CHANGE in conduction velocity
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How are the chemical senses of smell and taste different and similar?
Different stimuli (airborne stimuli in smell, but in taste- stimuli is conveyed to heir receptors by fluid) Separate receptors Distinct pathways Similarity - both chemical senses - in both systems, receptors are stimulated by the binding of chemical stimulants (odorants,tastings)
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Receptor mechanism of SMell
1) Olfactory transduction -CILIA of olfactory receptor neurons contain ODORANT RECEPTOR PROTEINS and are the SITE of olfactory TRANSDUCTION 2) Adaptation- In continuous presence of an odor, the olfactory response TERMINATES within about ONE MINUTE. 3) Receptor diversity -about 1000 receptor genes in rodents, 500 of that code for functional odorant receptors in HUMANS. Each code for ONE odorant receptor protein. Each protein HAS DIFFERENt ABILITY to bind odorant molecules. Each neuron express one receptor gene so 500 diff types of olfactory receptor neurons in humans
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What is the olfactory transduction cascade
1) Odorant binding to odorant receptor protein - G protein receptor belonging to superfamily METABOTROPIC -pass through membrane 7 times 2) Activation of Golf (Olfactory G protein)- Golf will stimulate ADENYLYL CYCLASE and INCREASE cytoplasmic cAMP concentration 3) OPENing if cyclic nucleotide gated ion channels (CNG)- cAMP binds and opens cation channel (Na+ and Ca2+). Inward current generates a DEPOLARIZING receptor potential 4) Amplification by Ca2+ activated Cl- channels - Calcium influx through CNG channnels stimulate Cl- permeable ion channel. The INWARD/depolarizing current created by Cl- EFFLUX further DEPOLARIZE the receptor neuron membrane if axon initial segment become depolarized above threshold, AXON will FIRE ****Cl- is EXCITATORY (Ecl is positive to threshold)
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WHy does adaptation of odorant receptors occur ? (2 reason)
1) MAIN REASON - ACTIVATION of signaling pathway within the olfactory receptor neuron ITSELF - Ca2+binds to calmodulin - Ca2+/Calmodulin complex inhibits CNG channel 2) PARTLY, due to odorant diffusion and transport away from the receptor in mucus OR BREAKDOWN of the odorant molecules by enzymes in the MUCUS
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Human can detect >20,000. Odors yet we only have 500 distinct olfactory receptor proteins. Each of these proteins have different molecular structure and different affinity for odorants and altogether can detect >20,000 odors. This is possible because of what?
POPULATION CODING - Each receptor neuron can be activated by SEVERAL DIFFERENT odorants with varying sensitivities - The effectiveness of a specific odorant varies, depending on the receptor protein present - The PATTERN of responses across the entire population of receptors is SPECIFIC for each type of odorant. - The response of an individual receptor is ambiguous but the population response is UNIQUE and reproducible evoking the same pattern of activities each time it s present
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``` Odorant concentration (intensity of smell) is coded by firing rate - higher odorant concentrations result in more rapid AP generation. The pattern (relative rates of firing among receptors) remains the same. This concept is known as? ```
FREQUENCY CODING
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Central processing of Olfaction 1) Olfactory bulb structure 2) Olfactory bulb processing
1) Axons of olfactory receptor neurons project to olfactory bulbs where they SYNAPSE with second order neurons called GLOMERULI -Each bulb contains >20,000 glomeruli **Glomerulus has : A) axon terminals of olfactory receptor neurons expressing the same receptor gene in one glomeruli (HIGH degree of CONVERGENCE increase the SENSITIVITY of olfaction) B) postsynaptic dendrites of second order neurons (mitral cells) 2) Axons are SORTED in olfactory bulb -all receptor neurons innervating one glomerulus contain the same olfactory receptor protein **Second order neurons (i.e glomeruli in olfactory bulbs) are connected by excitatory and inhibitory interneurons **Possible functions of olfactory bulbs: A) signal amplification (convergence of many receptor neurons) B) organize chemosensory input into categories C) output from the olfactory bulbs pass through the olfactory tracts directly to olfactory areas of the cerebral cortex
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How many bags taste can humans recognize? | Name them
``` 5 basic tastes SALT - sodium (other cations) SOUR - acidic H+ BITTER - Quinine SWEET - sucrose UMANI - glutamate A.A ```
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Mechanism of taste Gestation: sensory transduction Where are taste receptor cells found? What is the site of sensory transduction? What are the NT of taste receptor cells
Taste receptor cells are modified EPITHELIAL cells with distinct apical and basolateral membranes not neuronal -They are contained within TASTE BUDS which cluster into PAPILLAE on surface of the tongue - MICROVILLI on taste receptor cells are the SITE of sensory transduction * *Taste receptors cells make SYNAPSES onto afferent axons * **Individual taste receptor cells respond to stimuli belonging to one of the 5 basic category of taste (response depends on specific transduction mechanism present in APICAL membrane) * *Afferent response depends on response of taste calls innervated by the afferent (individual afferents fibers innervate MULTIPLE taste buds/taste receptor cells) -NTs are SEROTONIN, ATP/GABA
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Taste transduction occurs through what mechanisms? Which is ionotropic? Metabotropic?
IONOTROPIC - Sour (Acid) and Salt - Cations (Na+ and H+) diffuse through open ION channels on the taste cell apical membrane - Create inward current with depolarize the BASOLATERAL membrane (this membrane contains VGNa+ channels which further depolarize membrane) - This depolarization cause opening of VGCa+ channels METABOTROPIC - Sweet, bitter, UMANI - tasting molecules bind to G-protein coupled receptors which STIMULATE second messenger IP3 - IP3 stimulate TRPM3 (TRP family highly permeable to Ca2+) - IP3 also stimulate release of Ca2+ from the ER - Elevated level of intracellular CALCIUM triggers the release of transmitter (serotonin, ATP/GABA)
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Name the taste transduction this mechanism belong to -involves epithelial sodium channels (ENaC) which are DISTINCT from VGNa+ channels -These channels sometimes called AMILORIDE sensitive sodium channels ((Blocked by AMILORIDE compound) -ENaC channels are ALWAYS OPEN (Voltage insensitive) -type of LEAK CHANNEL
SALT TASTE transduction - Eat salty food, raise Na+ conc outside the apical microvilli, increase the Na+ driving force, cause Na+ influx into the receptor cell - INWARD sodium current depolarized the receptor cell, activate the VGCa+ channels, trigger transmitter release - ANIONS affect the salt response e,g NACL tastes saltier than Na-acetate. * *The GREATER the anion (acetate is larger than Cl-), the greater the INHIBITION if the salt response
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Name the taste transduction this mechanism belong to - Acidic food/protons - Proton flow in across the apical membrane through HH+ permeable cation channels that belong to the TRP family of channels - TRP channels stimulated to open by ACIDIFICATION
SOUR TATSE transduction -INWARD current of H+ depolarize the basolateral membrane, open VGCa2+ channels and trigger transmitter release to afferent axons
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Name the taste transduction this mechanism belong to - METABOTROPIC IN NATURE - The tasting molecule bind to GPCR, stimulate PLCb2, catalyze formation of IP3 - IP3 will a) activate the Ca2+ permeable TRP channel leading to Ca2+ influx b) release Ca2+ from intracellular organelles (SER) - Elevated intracellular CALCUM within cell trigger the release of transmitter (serotonin, ATP/GABA)
SWEET TASTE transduction
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Name the taste transduction this mechanism belong to - many POISONS - The ability to perceive toxic substances an this taste is an adaptation to prevent us form poisoning - taste cells contain a specific G-protein called GUSTDUCIN
- BITTER TASTE transduction | - SAME intracellular signaling pathways and transmitter release mechanism as sweet taste only a DIFFERENT receptor
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-Name the taste transduction this mechanism belong to - meaty/savory/pleasant - METABOTROPIC
UMAMI Taste transduction - same intracellular signaling and transmitter release pathways as bitter and sweet receptors - GPCR stimulate PLC, catalyze IP3 formation, Increase intracellular Ca2+, trigger neurotransmitter release
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WHat is the taste encoding mechanism How many tasting do individual taste receptor cells respond to? How any tasting do taste afferents respond to? What affect population coding here?
- Individual receptor cells respond to ONLY A SINGLE TASTANT - Taste Afferents respond to MORE THAN ONE tastant * *Some degree of Population coding exist - RESPONSES of single neurons become more SELECTIVE - which makes population coding less important
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WHat are the different ways to identify a specific food
TASTE TEMPERATURE TEXTURE ODOR - supplement taste
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How does the N.S sense position, movement and strength of muscle contraction?
By MUSCLE RECEPTORS - MUSCLE SPINDLES signal POSITION and MOVEMENT by monitoring muscle LENGTH - GOLGI TENDON signal STRENGTH/FORCE of muscle contractions
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Which sense organs are activated in neurological test?
TENDON TAP -activates MUSCLE SPINDLES that signal position and movement (not tendon organs)
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WHy is it essential to get a patient to relax in a neurological exam?
GAMMA motor neurons DYNAMIC) can change SENSITIVITY of 1a sensory neurons of Muscle spindles (DYNAMIC muscle cells only Receive 1a sensory neurons) -receive input in descending motor pathway which can cause increased reflexes in nervous patients **Hyper reflexia
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The problem with understanding the functions of muscle receptors is that they both have 2 opposite functions What are these functions ? What is the conduction velocity of muscle receptors?
1) CONSCIOUS function - signals from the muscle receptors reach the cerebral cortex/thalamus and produce conscious sensations * *conscious sense of body position - KINESTHESIA (you know touch the tips of your fingers under the table without looking) use PROPRIOCEPTION (sense of yourself) 2) UNCONSCIOUS function - muscle receptors make extensive connections in the SPINAL CORD that function WITHOUT requiring CONSCIOUS attention . These connections can produce AUTOMATIC/REFLEX reactions (adjust movement/posture without realizing it, MAINTAINING BALANCE when STANDING) **MUSCLE RECEPTORS have very HIGH conduction velocities
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How do you maintain balance when standing - compensate for perturbations?
- by REFLEX and COMPENSATORY REACTIONS (Unconscious sensation) - Stretch of muscle spindles evoke STRETCH REFLEX (Deep tendon reflex) in CNS that produce muscle CONTRACTION - This helps maintain Upright posture - Stretch reflexes are used clinically to evaluate NS function
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In GBS, what is affected? What happens in rare cases?
- Peripheral neuropathy- loss of axon in peripheral nerves - loss of neurons with large axons - loss of all PROPRIOCEPTION and no sense of body position IN RARE CASES NO motor deficits **Patient will then have to TRAIN themselves to walk again by using VISION (exteroception) to compensate for proprioceptive loss
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WHich of the 2 types of sensation help detect the OUTSIDE WORLD (e.g external receptors touch, temperature)
EXTEROCEPTION
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WHich of the 2 types of sensation help detect POSITION and MOVEMENT of body ITSELF
PROPRIOCEPTION **include muscle receptors (muscle spindle and Golgi tendon organs) and joint angle receptors
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Name the type of muscle receptors - specialized muscle cells that have both SENSORY and MOTOr innervation (gamma motor neurons) - sensory neurons sensitive to muscle stretch
MUSCLE SPINDLES * *signal muscle LENGTH, MOVEMENT, VELOCITY (change in length/time) - sensitivities are adjusted by gamma motor neurons * *tells location of e.g arm and how fast it is moving
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Name the type of muscle receptors - located in muscle tendons or connective tissue attachments - sensitive to tension in tendon
GOLGI TENDON ORGANS **Signal FORCE
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Name the 4 muscle properties
1) Muscle contraction 2) Isotonic contraction 3) Isometric contraction 4) Muscle tonus
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Describe the process of muscle contraction (one of the 4 muscle properties ) What happens to muscle length during contraction? ***How can can calculate the limb position and rate of limb movement
1) Skeletal muscle contracts when ALPHA MOTOR NEURONS (lower motor neurons) fire AP 2) When Muscle cells CONTRACT, they get SHORTER and generate FORCE. whole muscle also gets shorter; force is exerted on tendon or connective tissue attachment * *To calculate LIMB POSITION (joint angles) - know the MUSCLE LENGTH * *To calculate RATE of LIMB MOVEMENT - know how fast muscle length is changing (VELOCITY)- N.S does this
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Name the contraction type? - SAME FORCE - muscle CONTRACTS and moves MODERATE/CONSTANT load - e.g Lifting an object - LENGTH SHORTEN and TENSION/FORCE on tendon are CONSTANT - MUSCLE SPINDLES used primarily
ISOTONIC CONTRACTION * *Movement and position detected by MUSCLE SPINDLES * *Force detected by GOLGI TENDON ORGANS
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Name the contraction type - SAME LENGTH - Muscle contracts against immovable load - Force INCREASES greatly, tendon stretches slightly - tension on tendon is proportional to the force - No change in muscle spindles What detects this increased force?
ISOMETRIC CONTRACTION ** -INCREASED force detected by GOLGI TENDON ORGANS E.g Dr Zill trying to lift weights at YMCA - No gonna happen
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Muscle tension at rest is called? What is it due to ? How it is tested ?
MUSCLE TONUS -due to activities in alpha motor neurons at rest To TEST muscle TONUS 1) first tell pt to RELAX - muscle cells can easily be stretched in relaxed state 2) slowly STRETCH the muscle by moving limb at joints (PASSIVE STRETCH-physician Stretch the arm of pt) -MODERATE excitation of muscle spindles To Test muscle STRENGTH 1) compare tonus to normal muscle strength 2) tell pt to resist the stretch - contract muscle - ISOMETRIC CONTRACTION -muscle cells stiff (activated ALPHA MOTOR NEURONS) and hard to stretch -HIGH TONUS ** INCREASED TONUS is indicative of UPPER MOTOR NEURON DISORDERS
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1) Where are muscle spindles found? 2) what is their orientation to regular muscle cells 3) Number in different muscles? 4) Where are they found the most ? 5) what happens to muscle spindles when muscles are stretched? 6) what innervated spindle muscle cells
1) found inside muscle among regular muscle cells 2) PARALLEL 3) The number of muscle spindles vary in diff muscle - 20 - several 100 per muscle 4) High DENSITY of spindles in muscle that require FINE CONTROL - e.g small interosseus muscles of hand or extraocular muscles of eye that move the eye 5) Muscle spindles Stretch when muscles stretch due to PARALLEL orientation 6) muscle spindle cells are innervated by SENSORY neurons (cell bodies in DRG) and MOTOR neurons (cell bodies in VENTRAL HORN)
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1) what are muscle cells inside spindles called? 2) What are all regular muscle cells outside the spindle called? 3) How are the spindle cells specialized?
1) INTRAFUSAL cells 2) EXTRA FUSAL cells 3) 2 regions of intrafusal cells : * *POLAR/END regions - contractile filaments, CAN CONTRACT, location of MOTOR INNERVATION * *EQUATORIAL/MIDDLE region : - NUCLEI in the MIDDLE of cell - location of SENSORY nerve endings - No contractile filaments, DO NOT OCNTRACT
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What are the 2 types of INTRAFUSAL cells and how do they differ in their contractile properties?
1) FAST Conducting - Typically 1/spindle - contract RAPIDLY when activated - NUCLEI BAG CELLS, nuclei clustered in the center 2) SLOW conducting - typically 6-10/spindle - SLOWLY contract - nuclei CHAIN cells - nuclei arranged in a ROW
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How are spindle muscle cells innervated?
1) innervated by GAMMA MOTOR NEURONS (innervated only SPINDLE MUSCLE CELLS not regular muscle cells) - smaller than alpha motor neurons - form up to 30% of all axons in ventral roots - firing of GAMMA motor neurons cause the SPINDLE muscle cells to contract but DOES NOT generate much force at the muscle tendon * There is NO SELECTIVE VOLUNTARY CONTROL of gamma motor neurons ***Contraction of REGULAR muscle cells occurs through ALPHA MOTOR NEURONS and REFLEXES
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What are the 2 types of gamma motor neurons and what type of spindle muscle cells do they innervate?
1) GAMMA DYNAMIC motor neurons - innervate FAST contracting muscle cells 2) GAMMA STATIC motor neurons - innervate SLOW contracting muscle cells
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What happens when regular muscle cells contract verses when spindle muscle cells contract?
REGULAR/EXTRAFUSAL - They shorten SPINDLE/INTRAFUSAL - Polar (has contractile filaments shorten - Equitorial/middle part (no contractile filament) does not shorten but STRETCHES- little force is generated
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Overall, what are the 4 properties of SPINDLE MUSCLE CELLS
1) Specialization of intrafusal muscle cells - Equitorial/middle (no contractile filaments, HAs NUCLEI) - Polar ends (contractile filament, no nuclei) 2) Types of muscle cells in spindle - Fast contracting (nuclei big cells) - Slow contracting (nuclei in a row) 3) Motor innervation of muscle spindle - GAMMA MOTOR NEURONS (static-slow, dynamic-fast) 4) COntraction of muscle spindle - polar ends contract - middle ends stretch
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SENSORY innervation of spindle muscle cells 2 classification Name this - One per spindle - innervates ALL MUSCLE CELLS in muscle spindle (both fast and slow contracting) - LARGEST sensory axons in PERIPHERAL nerves - Very FAST conduction of AP
PRIMARY (1a) ENDING
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SENSORY innervation of spindle muscle cells 2 classification Name this - variable number per spindle (1-5) - innervated ONLY SLOW contracting muscle cells - FAST conduction (not as fast as the other sensory nerve ending)
SECONDARY (II) ENDING **Sensory neurons are found in the MIDDLE/ non-contractile part of the spindle muscle cells
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What innervate fast contracting muscle cells that’s only receive 1a SENSORY neurons not II
GAMMA DYNAMIC MOTOR NEURONS
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1) WHat sensory neuron responds best to STRECTH OF MUSCLE? Why? 2) WHen can muscle spindle cells be activated? 3) Which Sensory neuron encode MAGNITUDE of the change in LENGTH (how much the spindle has stretched) and are much LESS sensitive to VELOCITY 4) Which sensory neuron encode VELOCITY of stretch and also MAGNITUDE of the change in LENGTH
1) BOTH Ia and II 2) Muscle spindle cells activated by TENDON TAP -when muscle is relaxed -produces very FAST, SMALL lengthening of the muscle. This activate all spindle simultaneusly. Golgi tendon organ NOT activated 3) SECONDARY II 4) PRIMARY 1a
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You are standing in a moving bus and suddenly tilted forward? What is the main reason for this? What is active?
-SMALL RAPID change in length produced LARGELY form PRIMARY 1a sensory neurons. Very little firing from II * *SENSITIVITY TO VELOCITY produces LARGE bursts at start of perturbation, you are able to DETECT SWAY before LARGE MOVEMENT OF BODY OCCURS - Sensitivity can be enhanced by GAMMA MOTOR NEURONS
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1) What is the action of gamma motor neurons on muscle spindles 2) What else can be activated alongside gamma motor neurons? What is the result of this coactivation ?
1) Gamma motor neurons are used to adjust the spindle length to MUSCLE length (Spindle cells can signal STRETCH from any position) 2) Alpha motor neurons coactivation - Adjust and reset the muscle spindle length to ANY MUSCLE length * *Gamma DYNAMIC motor neurons SELECTIVELY enhance SENSITIVITY of 1a sensory neurons - if spindle muscle cells are TENSE, sensory endings will fire to a very small stretch..
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What has sensory endings that are SENSITIVE to FORCE of contraction?
GOLGI TENDON ORGAN *Innervated by Large (Type 1b) sensory neurons end in MUSCLE TENDON or CT attachment (MYOTENDINOUS junctions) -Branches intertwine with collagen fibers. Large forces applied to tendon cause it to become TAUT E.9 ISOMETRIC CONTRACTION **Firing is maintained as long as FORCE is developed
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What is the response of tendon organs to firing
- When muscles contract against a LARGE load (ISOMETRIC CONTRACTION), tendon organ FIRE INTENSELY - When muscles contract against a MODERATE load (ISOTONIC CONTRACTION), tendon organ firing reflects amount of force needed to move load. * *MUSCLE STRETCH or TENDON TAP DOES NOT excite tendon organs
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SUMMARY OF MUSCLE sensory RECEPTORs Name the receptor - One sensory neuron per sense organ - INNERVATES ALL MUSCLES CELLS (fast and slow contracting) - signal MOVEMENT, VELOCITY and LENGTH - GAMMA DYNAMIC MOtor neurons INCREASE sensitivity - GAMMA STATIC motor neurons INCREASE sensitivity
MUSCLE SPINDLE PRIMARY 1a
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SUMMARY OF MUSCLE sensory RECEPTORs - 1-5 sensory neurons per sense organ - INNERVATES ONLY SLOW contracting spindle muscle cells - signal LENGTH NOT velocity - GAMMA DYNAMIC has no effect - GAMMA STATIC INCREASE sensitivity
MUSCLE SPINDLE SECONDARY II
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SUMMARY OF MUSCLE sensory RECEPTORs - 1-2 sensory neurons per sense organ - INNERVATES muscle tendon at junction of muscle cells - signal muscle FORCE - GAMMA motor neurons have no effect
GOLGI TENDON ORGAN 1b
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Differentiate between MUSCLE SPINDLES or GOLGI TENSON ORGANS What happens when: You rapidly stretch a muscle that is relaxed ?
Muscle spindle -INCREASE discharge Golgi tendon Organ -Little or no increase
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Differentiate between MUSCLE SPINDLES or GOLGI TENSON ORGANS What happens when: -You try to stretch a contracted muscle
Muscle Spindle -No discharge Golgi tendon Organ -INCREASE discharge
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Differentiate between MUSCLE SPINDLES or GOLGI TENSON ORGANS What happens when: ISOTONIC contraction with alpha-gamma co-activate (normal condition) **Isotonic- lift an object, muscle length shortens, force is constant
Muscle Spindle -MAINTAIN discharge Golgi tendon Organ -DISCHARGE reflects LOAD
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Differentiate between MUSCLE SPINDLES or GOLGI TENSON ORGANS What happens when: ISOMETRIC CONTRACTION ** Isometric - attempt to lift immovable object, muscle length constant, FORCE is LARGE
Muscle Spindle -No discharge Golgi tendon Organ -LARGE INCREASE in discharge

Structure And Function 1 (4 decks)

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