Chapter 9&10 - Muscle Flashcards

(155 cards)

1
Q

What is coupling?

A

Sequence of events by which an action potential along the sarcolemma leads to sliding of protein myofilaments

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2
Q

Follow depolarization to the cisternae

A

First there is excitation with electricity…. By depolarization

Then this is coupled to sliding filaments of muscle contraction

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2
Q

Follow depolarization to the cisternae

A

Neuron depolarization: Na+ enters neuron cytoplasm in small steps to end of neuron,synaptic vesicles lyse at membrane of neuron, NT[ach] released into synaptic cleft of synapse

Synaptic cleft neurotransmitter transmission : Ach diffuses high to low, neuron to muscle

Skeletal muscle cell depolarization: NT/Ach binds @ motor end plate & starts local ion changes, opening Na+ channels-> muscle cell inside becomes slightly less negative=local graded potential

Depolarization/action potential sweeps down sarcolemma into T-tubule into cell [1-2 millisec]

Soooo cisterns release Ca++ which exits into cytoplasm

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3
Q

What is the sliding filament theory?

A

Thin filaments slide past thicker myosin so that actin & myosin overlap to a greater degree-> shortening of muscle

Heads of myosin attach to actin, and de attach->ratcheting motion;requires Ca++ [Ca++ rearranges troponin/tropomyosin with actin, freeing it to slide]

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4
Q

What is contraction?

A

Ca++ binds to troponin which then changes shape
Myosin binding sites on actin exposed
actin is “let go” & it slides into myosin
actin binds to myosin heads in cross bridges; using ATP to de-attach=ratcheting motion
muscle shortens=contraction

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5
Q

Explain the Cross Bridge Cycle, specific detail of myosin changes

A
  1. Cross bridge attachment (energized myosin attaches to actin)
  2. Working stroke (ADP and Pi are released, myosin head binds & pivots, pulling on actin)
  3. Cross bridge detachment (after new ATP binds to head, actin is let go)
  4. “Cocking” of myosin head (hydrolysis of ATP to ADP and Pi by ATPase gives energy and myosin head returns to high energy position, “cocked”)

Contraction (SLIDING) continues as long as there is Ca++ and ATP

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6
Q

How much do muscles shorten during contraction?

A

Muscles shorten 30 to 35%

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7
Q

What are the major events of relaxation?

A

Acetylcholinesterase (ACHase) on sarcolemma decomposes Ach
Muscle no longer stimulated
Ca++ moves from cytoplasm into sarcoplasmic reticulum
cross bridges break
actin slides back out of myosin

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8
Q

2 major facts about RELAXATION

A

Muscle lengthens

Troponin & tropomyosin hold actin

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9
Q

Relaxation & Contraction

A

Relaxation: when Ca++ is low in the cell cytoplasm [high in cisterns], muscle is relaxed & tropomyosin blocks actin
Contraction: when Ca++ rises in the cell cytoplasm, it binds to troponin, it changes shape, tropomyosin moves, and actin is freed to slide

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10
Q

Where does muscle get ATP for cross bridging in contraction?

A
  1. stored ATP in muscle cell
  2. stored creatine changed to creatine phosphate in muscle cell

These last a few seconds and cell must make ATP from glucose

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11
Q

What is Direct phosphorylation?

A

Coupled reaction of creatine phosphate (CP) and ADP, No O2 use, 15 seconds of energy

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12
Q

What is Anaerobic pathway?

A

Glycolysis and lactic acid formation, No O2 use, 30-40 seconds of energy

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13
Q

What is Aerobic pathway?

A

Aerobic cellular respiration, O2 REQUIRED, hours of energy!!!!!!!!!!!!!

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14
Q

In 6 seconds of short duration….

A

ATP stored in muscles is used first

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15
Q

In 10 seconds of short duration….

A

ATP is formed from creatine phosphate and ADP

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16
Q

in 30-40 seconds short duration…

A

Glycogen stored in muscles is broken down to glucose, which is oxidized to generate ATP (anaerobic)

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17
Q

Hours pf Prolonged duration exercise…

A

ATP is generated by breakdown of several nutrient energy fuels by aerobic pathway

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18
Q

How does muscle get glucose?

A

Liver and muscle change glycogen to glucose & delivers it to muscle through blood

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19
Q

How does glucose diffuse into muscle cell?

A

From BLOOOOOd

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20
Q

What in cytoplasm changes glucose to pyruvic acid (3C)?

A

enzymes

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21
Q

Glycolysis in muscle cell yield how many ATP?

A

2

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22
Q

what in glycolysis in muscle cell diffuses into mitochondria?

A

pyruvic acid

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23
Q

in krebs cycle/aerobic respiration in muscle cell….what changes to acetyl co-A?

A

pyruvic acid

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24
in krebs cycle/aerobic respiration in muscle cell....what enters krebs cycle?
co-A
25
in krebs cycle/aerobic respiration in muscle cell....what diffuses into cell?
O2
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in krebs cycle/aerobic respiration in muscle cell....what enters mitochondria & Krebs cycle couple with oxidative phosphorylations?
O2
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in krebs cycle/aerobic respiration in muscle cell....what are the products? (4) --->?
``` heat CO2 gas 36 ATP H+ ------------------->>>>>>> H2O ```
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How is O2 supplied for Krebs cycle?
1 Hemoglobin, blood protein in red blood cell releases oxygen to muscle cell 2 myoglobin a protein in muscle cell stores O2 from blood in muscle cell temporarily and releases O2 to cytoplasm when blood vessel clamped in contracting muscle
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What happens when O2 to cell runs out? EPOC
no more krebs cycle EPOC = oxygen debt = excess post exercise oxygen consumption when no O2, pyruvic acid decreases pyruvic acid cannot diffuse out of cell to blood so pyruvic changes to lactic acid to diffuse out of cell to blood blood carries lactic acid to liver
30
EPOC/ oxygen debt in liver
Liver runs glycolysis backwards: changes lactic acid back to pyruvic acid & adds ATP to change it back to glucose Therefore liver uses its ATP
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EPOC/oxygen debt in liver ..... body in oxygen debt until...
1 liver replaces its ATP 2 muscle replaces its creatine phosphate & original ATP 3 Mb O2 reserves replenished 4 glycogen replenished
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Contraction of a whole skeletal muscle, muscle tension
force exerted by contracting muscle on an object
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contraction of a whole skeletal muscle, load
force exerted on the muscle by the weight of the object
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contraction of a whole skeletal muscle,motor unit
a motor neuron and all the branches to muscle fibers it supplies
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contraction of a whole skeletal muscle, explain muscle and motor units
muscles exerting fine control have SMALL motor units, large motor units to large muscles with less precise control, like hip
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Force of muscle contraction affected by.....
1 number and size of contracting muscle cells 2 frequency of stimulation 3 degree of muscle stretch THE GREATER THE LOAD THE SLOWER THE CONTRACTION
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muscle twitch
response of motor unit to single action potential
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threshold stimulus
minimum strength stimulus needed for contraction, anything less than threshold gives no contraction
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all-or-none response
if muscle gets threshold stimulus, contracts completely if muscle gets greater than threshold, still contracts exactly same as threshold no PARTIAL CONTRACTION OF ISOLATED MUSCLE
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MYOGRAM
graph of single contraction of isolated muscle lasting fraction of second
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phases of twitch
``` latent/lag = period between threshold stimulus until contraction begins contraction= beginning to max contraction relaxation= max contract to NO contract REFRACTORY = period after stimulation & contraction in which muscle will not respond. can stimulate w threshold stimulus and no response ```
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tetany
sustained contraction; no relaxation period in skeletal
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fatigue
inability to contract muscle, increased LACTIC ACID; low ph, high K+ usually not lack of ATP
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cramp
prolonged spasms, LACK OF ATP, low ca++, drink h2O
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tone
relaxed muscles always slightly contracted
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rigor mortis :0
rigor of death muscles stiffen 3-4 hrs after death peak rigidity TWELVE HOURS Ca++ rises in muscle cells NO ATP FOR DETACHMENT OF ACTIN FROM MYOSIN rigidity decreases over 48-60 hours by bacterial degradation
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prime mover
muscle in a group responsible for most movement
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synergist
muscle in a group that assists prime mover
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antagonist
muscle in group that opposes prime mover
50
origin
point of attachment of one end of muscle that is relatively immobile
51
insertion
point of attachment of one end of muscle that moves
52
insertion moves toward origin during what?
contraction
53
origin-insertion nomenclature
stern0cleidomastoid , origin = first - sternum | insertion = last = mastoid process
54
points of origin in biceps
2 heads of origin (attachment)
55
size in pectoralis major is what?
large
56
_____ maximus and minimus?
big and little what? i like big ... butts
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deltoid is what shape? trapezius is what shape?
triangle; trapezoid
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the extensor digitorum does what action?
EXTENDS idiot
59
flexor digitorum probably...
flexes?
60
name the 2 types of contraction
isotonic | isometric
61
isotonic =
muscle shortens with contraction
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isometric =
muscle stays the same length with contraction
63
velocity of contraction (3)
slow OXIDATIVE fibers fast OXIDATIVE fibers fast GLYCOLYTIC fibers
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immobilization of muscles lead to what?
cell wasting or atrophy
65
resistance exercise cause what to happen to skeletal muscle?
hypertrophy or cell enlargement
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regular aerobic exercise leads to what 2 things?
increased ENDURANCE, increased STRENGTH
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Central nervous system
brain and spinal cord
68
peripheral nervous system
nerves that connect central nervous system to rest of body, afferent sensory and efferent motor (2) somatic and ANS
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automatic nervous system
one efferent part of PNS, divided into sympathetic and parasympathetic, that maintains unconscious homeostasis involuntary
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2 types of nerve tissue
neuron | neuroglial cells
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neuron
basic functional unit excitable; reacts to change transmits messages
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neuroglial cells
accessory cells variety of support function no impulse transmission
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central nervous cells
``` neuron neuroglial (half mass of brain small cells) astrocyte (star) oligodendrocyte microglia ependymal cell ```
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astrocyte (star)
support to neuron exchange with blood capillaries for neuron help form the blood brain barrier synapse formation
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oligodendrocyte
makes myelin sheath (CNS ONLY)
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microglia
phagocyte | assist injured neurons
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ependymal cell
lines ventricles of brain | help circulate cerebrospinal fluid
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PNS cells
neuron | neuroglial - satellite cell, schwann cell
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schwann cell
makes myelin sheath (PNS ONLY) | used in regeneration of axons
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anatomical types of neurons
multipolar bipolar unipolar
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multipolar neurons
``` many cytoplasmic extensions from cell body - 3 or more most common (99%) major type in cns function = motor or association ```
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bipolar neurons
``` 2 extensions from cell body function = special sensory (eye, olfactory) ```
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unipolar neurons
``` one extension from cell body function = sensory (GANGLIA) ```
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functional types of neurons
1 sensory 2 association = interneuron 3 motor
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sensory neurons
sensory receptors send messages through PNS to CNS (afferent) most unipolar sensory from organs = visceral afferent
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association neurons or interneuron
in CNS transmits messages from 1 part of CNS to another part of CNS multipolar
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motor neuron
from CNS to PNS (EFFERENT) multipolar carry messages to effector = muscle & gland
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2 main parts of motor neuron
somatic nervous to skeletal muscles | autonomic nervous to smooth, cardiac muscles, and glands
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neuron characteristics
amitotic extreme longevity high metabolic rate (ONLY SURVIVE FEW MINUTES WITHOUT OXYGEN)
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neuron structure (PNS OR CNS)
``` cell body with neuroplasm and organelles no centrioles... used in mitosis golgi well developed endoplasmic reticulium = NISSL BODIES nucleus: no reproduction after maturity PIGMENT INCLUSIONS - held in vacuole sac, lipofuchsin pigment is a sign of aging ```
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cell body has cytoplasmic extensions...
dendrite, axon
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clusters of cell bodies
in cns= nuclei | in pns= ganglia
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bundles of cell processes
in cns= tracts | in pns= nerves
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detail dendrites
short, highly branched enormous surface area for receiving signals from other neurons receptor for message= graded potential; conducts into cell body
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detail of axon
long and singular 1 per cell arises from axon hillock (trigger zone) near cell body generates and conducts messages away from cell body ex motor axons controlling great toe 3-4 feet long~@!@@@@@@!!!!!!!!
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more detail of axon
fine branching @ end is PRE SYNAPTIC terminal with synaptic knobs containing neurotransmitter NT that can diffuse into ECF when released has ALL the organelles of cell body and dendrite EXCEPT NISSL BODIES AND GOLGI, for protein packaging... so quickly deteriorates if cut
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use of what in axon aids movement of molecules in long axon in either direction?
use of microtubules, communication in cell
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certain viruses like polio can use this to invade cell body?
use the axon's same retrograde movement
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presynaptic terminal @ tip of axon
contain vesicles with neurotransmitter (NT) | releases NT to diffuse across synapse to next dendrite on 2nd neuron = synaptic transmission
100
synaptic transmission
dendrite neuron #1 -> cell body neuron #1-> axon neuron #1-> nt diffuses -> dendrite neuron #2->cell body #2-> axon #2
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role of myelin in PNS
white lipid-protein membrane of schwann cell wrapped around axon called myelin sheath (DENDRITES NEVER WRAPPED) EXTERNAL TO MYELIN SHEATH is neurilemmal sheath = rest of schwann cell, cytoplasm, nucleus, membrane
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neurilemmal sheath in PNS
increases impulse conduction | allows regeneration
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myelin and impulse conduction
as increased myelin, increase speed of transmission myelin is in patches on axon, each patch a SWANN CELL - naked axon in between is a node of rangier
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saltatory conduction
transmission can jump from node to node
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white matter in PNS
regions of brain and cord with dense myelination
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grey matter in PNS
cell bodies and unmyelinated fibers
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myelin & regeneration in PNS
if axon is severed, all except sheath distal to cut is DECOMPOSED proximal axon sprouts cytoplasm & seeks tube of sheath for path to muscle if sprout enters sheath, then axon can re-grow sheath shows path to growing axon until finds muscle or gland
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regeneration in CNS
no neurilemmal sheaths in CNS no axon regeneration adult neuron does not divide cut through cell body, in PNS OR CNS BRINGS CELL DEATH!!!!!!!!!!!!!!! limited growth with fetal tissue implants
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neurophysiology: resting membrane potential
AT REST ( NO MESSAGE TRANSMITTED) membrane is charged so outside positive with respect to inside
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how can ions move to create this imbalance in resting membrane potential?
respond (open/close) to pressure/voltage/chemicals each channel selective for ions to pass so can permit unequal distribution or ions in ECF vs cytoplasm
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RMP
NA + higher outside K+ higher INSIDE cytoplasm= 150 mm k+ and 15 mm na+ ECF= 150 mm Na+ and 5 mm k+
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if add all charges in ECF nD COMPARE to all charges in cytoplasm, greater positive charge outside than inside where?
AT MEMBRANE
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at the membrane for RMP...
cytoplasm is neutral, elf is neutral ECF not elf
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potential across membrane is what #
~-70mV
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hyper polarizing agents
chemicals that affect RMP and make it more negative > -70mv more difficult to fire message (action potential) on that nerve patient has more difficulty responding
116
hyper polarizing agents affect what?
they affect RMP and make it more positive (+) than -70 e.g. -60, -50 nerve message fired more easily eg. caffein (in chocolate, colas, pepper, tea, coffee, mountain dew
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generating action potential
RMP- voltage gates closed for Na and k depolarization- increase in membrane na permeability and na moves from ECF into cytoplasm in small steps & once reaches threshold becomes self generating repolarization
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2 types of signals produced by change in membrane potential
graded potentials | action potential
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graded potentials
incoming signals operating over short distances, short lived; can initiate action potential
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action potential
long distance messages=rapid series of depolarizations and depolarizations; don't decrease in strength with distance ----- often graded potential change to AP at hillock
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depolarization
the membrane potential moves toward 0 mv the inside becoming less negative and more positive
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hyperpolarization
the membrane potential increases, the inside becoming more negative
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the key players
voltage gated Na+ channels and k+ channels
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repolarization
k+ exits membrane in a linear pattern directly behind Na+ movement restoring original resting potential na+ blocked occurs in small steps Na+/ka+ pump restores ion distributions of original RMP
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the events 1-4
resting state depolarization depolarization hyperpolarization
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the events 1-4 explained
no ions move through voltage-gated channels then na+ flows into the cell then k+ flows out of the cell then k+ continues to leave the cell
127
threshold response
depolarization when AP becomes self generating ---- graded potentials add at hillock
128
all or none response
AP happens completely with threshold stimulus or not at all
129
refractory period
period of open Na+ channels in which neuron cannot respond to another stimulus
130
synapse
junction that mediates information transfer ex axodendritic - btwn axon/dendrite presynaptic neuron= neuron conduction impulses toward synapse
131
postsynaptic neuron=
neuron transmitting electrical signal away from synapse
132
electrical synapse=
less common, protein channels between neurons, like gap junctions, synchronous activity
133
chemical synapses
depolarization releases Ca++ that opens vesicles in axon terminal that releases NT-> diffuses across synapse to receptor on next dendrite
134
in chemical synapses after few milliseconds NT
terminated by enzymes or reuptake by astrocytes or cell or diffusion away
135
the rate limiting step of message is much slower in what?
much slower in synapse, 150 m/sec is .3-5.0 m/sec
136
excitatory post synaptic potential EPSP
neurotransmitters that hypo polarize & excite next neuron with graded responses - may trigger hillock - AP
137
inhibitory post synaptic potential IPSP
inhibitory neurotransmitter that hyper polarizes next neuron-> less likely to fire
138
esps can add together to increase what?
threshold depolarization
139
temporal
rapid accumulations in time of presynaptic impulses
140
spatial
many neurons add together to stimulate the post synaptic neuron
141
neurotransmitters
chemicals released from end of axon that carry message of depolarization through synapse to next neuron have specific receptors on post neuron ex: ACH- degraded by a chase to choline and reused to make ash all skeletal muscles CNS monamines/biogenic amino acids (eli,norepi,serotonin,dopamine) some amino acids -- glycine, GABA, aspartic acid
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monamines/biogenic amino acids -- eli, norepi, serotonin, dopamine
broad distribution in brain inhibited by monamine oxidase diet can affect monamine production
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some peptides
neurotransmitters - strings of amino acids can enhance- substance P transmits pain can inhibit message: endorphins and enkephalins inhibit pain
144
neurotransmitters: some can excited or inhibit
ash excites skeletal muscle and inhibits cardiac muscle
145
neuromodulators
chemicals in the synapse that can alter the message of the transmitter NO nitric oxide
146
convergence of a message
action potentials of several neurons converge at synapse many neurons converge to fewer neurons used to go from sensory ons into cps
147
divergence
action potential of one neuron synapses into several neurons | CNs --> motor effectors (can take same message to may parts)
148
neuronal pools=
functioning group of millions of neurons in CNS if presynaptic neuron branches @ synapse, it will excite some post neurons in discharge zone and facilitate or help other neurons reach a threshold facilitated zone
149
patterns of neural processing- SERIAL
predictable patter of stimulation of one after another after another like spinal reflexes or serial killers
150
reflex arc
automatic unconscious response to change inside or outside body
151
reflex arc
maintains homeostasis 4 or 5 parts sensory neuron -> interneuron in CNS-> motor -> effector (muscle or gland)
152
reflex arc simplest
knee-jerk (2 neuron); unipolar in & multipolar out (no interneuron
153
parallel processing
input segregated into many different pathways simultaneously
154
nerve fiber classification
nerve fibers classified according to diameter, degree of myelination, speed of conduction