Unit 3 🧠🫀💪🏻 Flashcards

(138 cards)

1
Q

Propioception

A

Ability sense relative position of body parts

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2
Q

Neuron v glial cells

A

Neuron : signaling unit (most function of nervous system) function al unit transmits information from one cell to another
Amniotic (can’t divide except olfactory neurons and the hippocampus regions of the brain) (maybe to preserve learning)
Have high metabolic rates and last a lifetime amount

Glial cell : support unit

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3
Q

CNS v PNS

A

Central nervous system: associated with neurons involved in central processing located in the brain and spinal chord

Peripheral nervous system is associated with sensory input(afferent) and motor output (efferent) and connects the cns to to the body

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4
Q

PNS CNS control system system

A

Stimulus receptor afferent pathway control center efferent pathway effector response

PNS takes info form receptor to the CNS the control center which then makes a decision and sends an efferent message again the the PNS to effector which then triggers a response

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5
Q

Somatic nervous system

A

Efferent neurons

Voluntary movement of skeletal muscle

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6
Q

Autonomic neurons

A

Efferent neurons
Involuntary
Heart lungs glands etc and smooth muscles

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7
Q

Sympathetic

A

Autonomic
Involuntary
Activates the flight or fight response

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8
Q

Parasympathetic nervous system

A

Autonomic
Involuntary
Reverses the flight or fight response and helps body return to normal

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9
Q

Enteric nervous system

A

(Semi independent)
Autonomic NS
Controls GI tract
It can run independently or through modulation
Contains more more neurons the. The entire spinal chord

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10
Q

Soma

A

Cell body

Is the portion of the cell that Surrounds the nucleus and plays a role in protein synthesis

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11
Q

Dendrites

A

Short branched
Process that extends from cell body
Function to receive information
Neurotransmitter receptors

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12
Q

Axon

A

A large process that extends from the cell body
Point of origin called the axon hillock
Sends information via action signals
Axons contain micro tubules and are surrounded by myelin which surround the axon speeding up the propagation of the action potential

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13
Q

Anterograde transport v retrograde transport

A

Antero away from soma

Retro back towards soma

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14
Q

Axon terminals

A

Ending sections of the axon

Coverts the electrical signal into chemical signal (synaptic transmission) system

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15
Q

Multi polar

A

See figure 2

The normal one

Has many dendrites and one axon coming out
99% are multipolar

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16
Q

Bipolar neuron

A

Have only two processes that extend in opposite directions one is a dendrite the the other is axon

Retina of eye and olfactory system

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17
Q

Unipolar neuron

A

Have a single short process that extends from the cell body and branches into two or more processes that extend in opposite directions

Process that extends peripherally is called peripheral process and is associated in sensor reception

Process that extends toward CNS is the central process

Found in afferent division of PNS

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18
Q

Sensory neurons

A

Afferent neurons transmit info from sensory receptors towards the cns almost all sensory are unipolar

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19
Q

Motor neurons

A

Efferent
Transmit info from CNS toward some sort of effector
Typically multipolar

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20
Q

Inter neurons

A

Are located between sensory Neuron and motor neuron pathways
Involved in signal integration
Confined within cns

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21
Q

Astrocyte

A

CNS

Controls environment around the neuron

Lots of processes that tap around the blood vessels

Glycogen storage

K+ permeability

Gap junction

Neurotransmitters

Growth factors

Blood flow

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22
Q

Astrocyte glycogen storage

A

Helps store glycogen for metabolic processes and supplements the main source of auger the blood glucose level this extra storage can sustain the cns for 5to 10 min

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23
Q

K+ permeable of astrocyte

A

Active neurons loose k+ to outside which would act as a positive feed back if not for astrocyte

Take up k+ by a pump (sodium potassium pump) or cotransporters NA k cl and k cl exchangers

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24
Q

Gap junctions astrocyte

A

Coupled to each other as well as other glial cells through gap junctions

Helps modulate activity and sensitivity of cns

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25
Astrocyte neurotransmitters
Synthesize 20 different neurotransmitters and take up excess neurotransmitters to help terminate signal at synapse
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Astrocyte Growth factor
Secrete a variety of growth factors which are important in establishing fully functioning excitatory synapses
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Astrocytes blood flow
Modulate blood flow I the brain by inducing vasodilation and constriction this can occur through gap junction between astrocytes and endothelial cells of brain blood vessels
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Oligodendrocytes
CNS Maintain myelin sheaths Which insulates and propagates along the axon without being spread to other axons 15-30 processes Between each raping are nodes of ranvier Create salutary conduction And help cluster volatge gaskets NA channels at the nodes Regulate ph of cns
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Multiple sclerosis
MS is a autoimmune disease where the body attacks oligodendrocytes resulting in reduction of myelin Which can decrease conduction speed Which can result in loss of sensory perception and motor control 2x in women then men
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Ependymal cells
Line cavities of cns They produce cerebral spinal fluid and are important barriers between the csf and brain extracellular space these cells beat their cilia to help circulate spf
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Micro glial cells
Rapidly activated in cns in response to injury Injury causes them to change shape and become phagocytic Important I. Presenting antigens and lynphocytes in response to infection. Although helpful they can also be toxic to neurons and can result in long term damage Some medical interventions inhibit microglial activity
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Schwann cell
PNS Myelinating cell Provides myelin for only single segment of axon Myelin appearance and function the same in PNS and cns
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Satellite cells
Help maintain external chemical environment of PNS Very similar to astrocytes in CNS But in addition are highly sensitive to injury and inflammation
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Synaptic transmission
Movement of signal across synapses via neurotransmitters
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Chemical synapses
Occur when neural membranes are very close together but remain distinct, leaving space Use neurotransmitters to communicate Pre and post terminals contain things to send and receive signal Pre contains large amounts of vesicles packed with neurotransmitters when action p arrives opens ca channels which trigger then induce exocytosis on neurotransmitters The nuerotrans then bind to receptors on post and induce confirmational shifts which causes the receptor to act like a pore letting in ions Enzymes break down neurotransmitters turning off the signal the parts of neurotransmitters are then retaken by pre terminal and sent back to soma Ex of enzyme that turns off is acetylcholinesterase that breaks down the neurons transmitter acetylcholine
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Electrical synapses
Over when membranes are linked together (gap junction) via specialized protiens (connexins) Allow corn flow of ions quickly from one cell to another Ex heart muscle
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Presynaptic termial
Part that releases neurotransmitters into synaps
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Postsynatpic terminal
Part of neuron the recives neurotransmitters on other side of synapse
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Synaptic cleft
Narrow space between the pre and post terminal
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Effect on post synapse excitatory and inhibitory Epsp Ipsp
Last for a few seconds and the. Potential goes back to resting Normally not sufficient alone Excitatory Epsp- depolarization - enough change to set off action potential Inhibitory Ipsp- hyperpolarization - This occurs at axon hillock
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Special summation
The many epsp and ipsp combine at the soma which results in a much larger voltage charge
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Temporal summation
Many epsp from the same synapse can also combine if they arrive in taped succession
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Post synaptic receptors
Hundreds of different neurotransmitters and receptors Types : Chemically gated ion channels When open the item type will determine which ion flows in and whether it is epsp or ipsp Second message systems results in cascade of of interactions the type of cascade will result in either an excititory response or inhibitory
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Excititory synapse
Most I. The brain use glutamate or apsarate as neurotransmitters Bind to non selective cat ion channels that allow for NA or k to pass Many of these can f Reach threshold and create action potential
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Long term potentiation
Subset of synapses Capable of forming memories by increasing strength and and activity of synapse Involves glutamate and a receptor known as NMDA receptor ( unique in that it is both ligand and voltage gated) When activated by ligands become permeable to NA if the charge is suffecient becomes permeable to ca as well Which triggers a second messenger cascade that results in an increase in the number of glutamate receptors which the. Increases strength of the synapse It can last for months weeks or even years wether or not synapses is continually used
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Inhibitory synapses
The excitability is governed by neurons is essentialy governed by balance of excite and inhibitory Main neurotransmitters are GABA and glycine both bind to receptors that result in the increase of conduction of cl because it is - and moves into the cell makes it oppose depolarization
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Modulatory synapses
Are those that can be primed by neurotransmitters so they are able to respond more powerfully to other inputs For example norepinephrine (has little effect alone) but when exposed first to norepinephrine reacts more powerfully to glutamate
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Functions of muscles
``` Movement Maintenance of posture Respiration Heat generation Communication Constriction of organs and blood vessels Pumping blood ``` More ex. Protect fragile organs Maintains integrity of body cavity And more
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Muscle function movement
Skeletal muscles yank and pull on out skeleton resulting in movement
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Maintenance of posture function o muscle
Without much conscious control muscles generate contractile force that allows them to maintain an erect or seated position also known as posture
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Respiration function of muscle
Via diaphragm air is driven into and out of body
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Heat generation
Contraction of muscles generate heat which helps maintain homeostasis
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Muscle function communication
Allows us to talk write gesture and convey our emotional state
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Muscle function constriction of organs and blood vessels
Nutrients move through our digestive system urine is passed out of the body and and secretions are propelled out of glands by contraction of smooth muscle Also constriction of blood vessels regulate bp
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Pumping blood function muscle
Heart pumps blood through the body
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All muscles have the following properties
Contráctility: the ability for the muscle to shorten (for one muscle to contact another must extend) Excitability: has the ability to respond to a stimulus when delivered from a motor neuron and hormone Extensibility: the ability for the muscle to be stretched (lack of extensibility is spasticity) Elasticity: ability to recoil or bounce back to the muscles original length after being stretched
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Skeletal muscle
``` Striated Voluntary 40% of our weight There are many nuclei in each skeletal muscle cell which are pressed against the sarcolema because of all the myofibrils And myofilaments ```
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Smooth muscle
Wildly distributed throughout body Found in hollow organs tubes and blood vessels, airways inside the eye Lacks striations Involuntary Aka visceral muscle Autorythmic
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Cardiac muscle
Only found in the heart Striated Involuntary Autorhythmic : capable of contracting spontaneously or without neurosurgeon or Hormonal input
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Muscle fiber
Skeletal muscle cell which develope as many myocytes fuse together Same diameter as hair follicle
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Fascicles
Are bundles of muscle fibers | Are supplies with a rich network of blood vessels and nerves
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Muscle (structure)
A bunch of fascicles rapped together
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Structure ct muscle big to small
Epimysium - dense fibrous ct that surrounds out side of muscle Aka fascia Perimysium - surrounds individual muscle fascicles Endomysium surround individual muscle cells Loose areolar ct All are continuous with each other and come together at ends to form tendons ( muscle to bone )
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Muscle cell structure from big to small
Deep to endymsium Is sarcolemma : cell membrane Sarcoplasm : cytosol which contains large amounts of glycogen and myoglobin (red pigment that stores o2 like hemoglobin) Myofibril (rod like protien structure that takes up most space) 80% Can contain hundreds and thousends Each myofibril is made up of myofilaments : protien molecules And each myofilaments can be divided into a sarcomere : contractile unit
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Myofilaments
Make up myofibrils | Forms striation due to regular organization and pattern
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A band
Dark area A in “dark” Anisotropic Where there is thick filaments and thin filaments
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I band
Light segments I in light Isotropic Where there is only thin filaments
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Z line/ disco
Are the deviations between sarcomeres Sarcomeres are connected z disk to z disk and connect form one end of muscle to the other Composed of alpha actinin which lets thin filaments attach
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H zone
Found I. The middle of a band (light zone usually center of sarcomere) Is only thick filaments
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M line
Dark line i between h zone that is in the middle of the a band Composed of myomesin that holds myosin in place
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Thick filaments
Are made up of myosin
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Thin filaments
Made up of actin
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G actin F actin
F actin - 2 strings of g actin wound together in helix G actin individual actin molecule contains binding site. (Pearls)
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Tropomyosin
Is a long string like polypeptide that runs along the f actin Hides or exposes binding site on g actin Long enough to cover the active sites of 7 g actin
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Troponin
Contain 3 globular proteins Troponin I Troponin T Troponin C There is one troponin for ever tropomyosin stand
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Troponin I
Binds to actin
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Troponin T
Bonds to tropomyosin | And helps position troponin on f actin
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Troponin c
Binds calcium ions What calcium binds to it it causes confirmation all shift of entire complex that results in exposure of myosin binding sites
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Myosin
Thick filaments Made up 300 myosin And each myosin is made up of 6 protien subunits 2 heavy Chains and 4 light chains Heavy chains look like golf club which is where head attaches Half of heads point up half down Center is only heavy chains
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Hinge region
Is the connection between the head and shaft of myosin Can bend Creates the power stroke in muscle contraction
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Myosin head
Has an ATPase that binds and hydrolysis atp into adp Atp provides energy for contraction Each head is associated with 2 tails Each thick filaments can interact with 6 thin filaments Bc head every 60 degrees Every thin can go with 3 think This means there are two thin for every thick 👍heads can bind to active sites on g protien molecules and form bridge The heads are attached to rod like portion of heavy myosin The heads have ATPase which lets the break down atp allowing it to bend and detach the myosin from the actin
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Cross bridges
The myosin heads link to the thin filaments that cause the the myofilaments to slide over each other Results in shortening of sacromere
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Titin
Is super long name (biggest protien in human body) Extends from z disc to m line Forms core of thick myofilaments Holds them in place and keeps the a band structured Can stretch and recoil Prevents over stretching and damage Returns muscle to normal Length Responsible for elasticity
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Dystrophin
Located between the sarcolema and outermost filaments Acts like an integral membrane protien and connects links the muscle cell to the endomycium May cause MD muscular distrophy And affects boys Most become wheel chair bond by 12 And die due to breathing difficulty by age 20
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T tubules
Invaginations They communicate extra cellular space and are fille by extracellular fluid They are located where the a and I band overlap Flanked on either side by the sarcoplasmic reticulum
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Sr sarcoplamic reticulum
Elaborate network of smooth endoplamic reticulum that surrounds and encases each myofibril It store calcium Which can be released when action potential is conducted along the sarcolema Runs parallel with myofibrils However there are enlargements at the a band I band junctions aka terminal cisternae
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Triad
One t tubule with two terminal cisternas on both sides Critical in muscle function Contains large amounts of voltage dependent protiens calles dihydropirdine (DHP)channels or L type channels
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DHP and l type channels
Although called channels they do not allow calcium to move through but rather they are linked to calcium channels called (cells RyR) Ryanodine receptor channels When membrane depolarizers the DHP detects signal which opens RYR releasing ca terminal cisternae to sr
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Neuromuscular junction😩👍😢
8 steps and they all suck
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Sliding filament model
The muscle contraction and shortening occur when myofilaments grip each other slide past each other and shorten sarcomeres The proteins don’t shorten Both Hzone and I band appear to be shrinking and A band doesn’t appear to shrink
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Neuromuscular junction step 1
Action potential arrives at axon terminal (Skeletal muscle no stimulation by neuron means no contraction) The axon delivers signal to neuro muscular junction (synapse)
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Neuromuscular junction step 2
The arrival of the actionpotential at the termial stimulates ca2+ ion voltage gated channels to open Ca2+ moves into cell from outside the cell
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Neuromuscular junction step 3
The axon terminal contains synaptic vesicles fellow with the neurotransmitter acetylcholine ACh Increased levels of Ca2+ triggers exocytosis and it releases ACh into cleft
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Neuromuscular junction 4
ACh diffuses across the synapse binding to the acetylcholine receptor On the ligand gated ion channels (nicotinic type 1) in the sarcolema of the post synaptic tissue aka the motor end plate ( location of ACh receptors)
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Neuromuscular junction step 5
ACh binding causes ligand gated NA K channels to open these channels are more permeable to NA so it depolarizers the sarcolema Which then causes the voltage gated NA channels to open initiating an action potential that spreads out from neuromuscular junction Travels down sarcolema but also down t tubules (Filled with extracellular fluid so high NA but low K) ACh receptors or ligand channels allow NA into the cell activating voltage gated channels Generation and propagating action potential
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Neuromuscular junction step 5a
Meanwhile for the muscle to relax ACh is removed for binding site Via an enzyme called acetylcholinesterase. Which splits ACh into two components acetyl and choline which diffuse out of cleft Choline which is essential nutrient. In vitamin B group (b4) is taken up by the axon terminal where it is recycled Our bodies can produce choline but we also need to eat it to have enough
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Neuromuscular junction step 6
The action potential does its thing 😉
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Neuromuscular junction step 7
Action potentials spread across sarcolema and t tubules The change in potential causes other voltage gated channels in t tubule to respond Dihydropyridine DHP Or L type gated channels which are mechanically linked to ryadine receptor channels (RyR) Which are calcium channels located I the SR membrane These two protein channels spans the distance t tubule and terminal cisternae In response to change in potential the Ltype or DHP cause the RYR to open letting ca ions go from the sr and diffuse into sarcoplasm These calcium ions bind to troponin causing it to move the tropomyosin molecules exposing the active sites on the g actin
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Neuromuscular junction step 8
When active sites are exposed it allows the formation of cross bridges In resting state myosin head is cocked And ready to go (it has adp and phosphate attached to it) the binding of actin causes the phosphate to detach from myosin head. Resulting in the release of energy which causes the myosin head to bend aka power stroke which forcefully pulls the actin past the myosin Although half point one direction and the other half the other, they all pull myosin toward the middle (shorten sarcomere)
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Step 9 of neuromuscular junction
In order for significant shortening to occur Head must detach And reattach on new site Head binds with atp molecule which detaches the head ATPase rehydrolizes the atp into adp and p and causes the head to recock (the recovery stroke) preparing it for the next power stroke During one muscle contraction this bridge cycle happens many times
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Cross bridge cycling
The attachment and reattcent of myosin heads and actin Happens asynchronously meaning not all at the same time and all heads will be at different stages Phase 1 power stroke or working stroke where myosin heads bend and retract the actin molecules Phase 2 the recovery stroke : Where the myosin heads detach from actin and are cocked back into high energy position the prepare for next stroke
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Relaxation of muscle
Begins when ACh is no longer being released The ACh that is in the synapse is breaker down by acetylcholinesterase Ending the action potential which stops the flow of ca out of the SR which allows the tropomine and tropomyosin complex to relAx blocking the active sites which prevents the cross bride cycle
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Muscle contracture
Occurs when muscle shortens and resists relaxing Long term / permanent contractons Causes include (prolonged immobilization) spasticity(spasm) and muscle weakness Temporay (rare) causes include servers muscle fatigue, resulting In physiologic contacture. Extreme exercise may lead to depleted atp which prevents the myosin head from detaching and muscle stays rigid
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Rigor Mortis
Is also caused by lack of atp when body dies Death It may take hour to fully develop Breakdown of SR and leakage of ca which initiates cross bridge formation how ever because there is no atp the heads don’t unbind and muscles become rigid
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Muscle cramps
We don’t know Contráctures are electrically silent or in other words we don’t see repeated action potentials coming down the motor neurons. It occurs because of a physiological change in the fiber itself and not the motor neuron Cramps are associated with many action potentials Most commonly found in the leg and foot Poorly understood
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Motor units
Motor neurons that are connected with skeletal muscle are called alpha motor neurons It divides into several branches Each innervating a muscle fiber One alpha neuron and all the fibers it innervates is known as a motor unit The size of motor units varies In muscle involved in fine movement there are about 3 to 5 muscle fiber per neurons ex eye and hands Muscles involved in powerful but less coordinated movemts have large motor units with thousands of muscle cells per neuron Legs and back
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Muscle twitch
The contraction caused by a single action potential The latent period - lag phase, is short 1-2 msec from when action potential reaches muscle until tension can be observed which is the time it takes fo ca to diffuse out of the sr and bind with tropomine moving the tropomyosin which allows for bridge formations to occure Contraction phase is period of time when the muscle is generating tension and is associated with the cycling of bridges Relaxation phase the time when muscle moves back to normal length Muscle units randomly fire creating smooth action potentials because they are not all going at the same time Even at rest some muscle fibers randomly fire
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Muscle tone
Due to muscle twitch firing even when muscle is relaxed causing the muscles to never completely relax even when asleep Takes up slack Deters atrophy
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Flaccid paralysis
When neuron to motor unit is cut and there is no electrical impulse to muscles causing them to become flaccid
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Isometric contrarion
When tension of the muscle increases without a corresponding Chang of length Important for maintains posture
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Isotonic contraction
Is when tension stays relatively the same and length changes Can be classified into Concentric Eccentric concentration
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Concentric
Isotonic If muscle generates tension and entire muscle shortens Curling a weight your bicep would be concentric contraction
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Eccentric contraction
ISOtonic When muscle is generating force but muscle is lengthening Works to decelerate the movement of the joint Can generate more force then concentric contraction. Better to train both Essentric can cause more tearing resulting in more soreness
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Muscle size and muscle growth
Muscle size is determined by the number and size of myofibrils which is also determined by the amount of myofilaments Resistance training causes an increase in myofilament protien production Caused by small microtares on the micro filament level It also causes there to be more connective tissue Endurance trading does little for muscle size but helps increase its ability to produce atp aerobically
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How to generate more forever in contraction
More motor units are recruited We are only able to use about 1/3 of our motor units As fiber is fatigued they are replaced by other groups to allow for a longer contraction time Only in rare circumstances can we use more motor groups which allows us to lift cars off of children
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Wave summation and tetanus
There is not refractory period so it can be re stimulated at any time meaning you can restimulate the same neuron with higher frequencies you would observe a gradual increase in force It would get to a point where it becomes so high that it doesn’t have enough time to relax which would cause tetanus Not enough time to remove calcium form charol creating maximum force
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Length tension relationships
If starting length is short the muscle has less room to contract making it a very weak contraction Or if it stretched to the point where actin can’t touch myosin then less force will be generated The best place is to allow every head to contract and contact actin and the sarcomere has the greatest distance to shorten
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Energy source of muscle contration
Ultimate source is atp Cytosolic atp Creatine phosphatE Glycolysis Aerobic or oxidative respiration
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Cytosolic atp
Floating pool of atp Present in cytoplasm Atp doesn’t require o2 to produce Immediate but short lived Few seconds of maximal activity Not good long term Good for small like eye contraction
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Creatine phospate
Once cytosolic atp is gone High energy compound Rapidly transfer phosphate to adp creating atp fast Without o2 Requires creatine kinase (located on m line of sarcomere) Can replenish atp pool several times Only gives 10 sec mor time Very common supplement only good for very small very specific activities
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Glycolysis
Is the break down of glucose Primary source from glycogen Can happen without o2 Major source during anaerobic activity Only can sustain about a minute
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Aerobic or oxidative respiration
Metabolic mechanism in the mitochondria Produces a lot more atp Lasts much longer then a minute Needs o2 Slower No fast for intense Moderate works 👍 Nutrient of choice is fatty acids
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Muscle fatigue
When the muscle is no longer able to contract optimally
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Central fatigue
The uncomfortable feeling you get when working out Psychological fatigue Factors realice to signal the brain that it’s tired Occurs well before the muscle can no longer contract
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Peripheral fatigue
Can occur anywhere between the neuromuscular junction Low frequency : marathon running Impaired ca release due to excitation coupling contraction problems Recovery 24 to 72 hours ``` High-frequency Circuit training Impaired membrane excitability As a result from imbalance of ions Causes inadequate NA k pump inactivation NA channels and impairment of ca channels Quick recover about 30 min ``` Other possible factors include Accumulation of inorganic phosphates To much hydrogen ion and ph change Glycogen depletion Imbalances in k Not on the list is lactic acid it does not cause fatigue or muscle soreness
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Slow twitch | Oxidative type I
``` Myosin ATPase activity slow Size small Duration of contraction long Serca pump activity slow Fatigue resistant Energy utilization aerobic/oxidative Capillary density: high Mitochondria: high numbers Color: red (contain myoglobin) ```
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Fast twitch oxidative type llA
``` Myosin ATPase activity fast Size medium Duration of contraction short Serca pump activity fast Fatigue resistant Energy utilization both Capillary density medium Mitochondria medium numbers Color red contains myoglobin ```
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Fast twitch glycolytic tips IIX
``` Myosin ATPase activity fast Size large Duration of contraction short Serca pump activity fast Fatigue easily fatigued Energy utilization: anaerobic glycolytic Capillary density low Mitochondria low numbers Color - white no myogloben ```
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Slow v fAst fibers
Slow twitch (ex deep calf) - good for standing Fast twitch(eye muscles)- good for sprinting Most muscles contain both Women seem to have higher ratio of slow twitch to fast twitch Default is type 1 Small neurons induce slow type Large myelinated fibers induce fast type Frequency of firing rates can also change type Generally genetics plays biggest role in type of fiber Training may be able to slightly alter ratios
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Agonist
A drug that has the same effect as a neurotransmitter
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Antagonist
Drug that blocks the effect of neurotransmitter
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``` Neuromuscular blocker (drug) 😀 ```
Ex tubcurarine ( comes from South America plant used for arrow poison) Alpha bungarotoxin (snake poison) pancuronium (lethal injection drug) Acetylcholine receptor antagonists Result flaccid paralysis
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Neuromuscular blocker(drug)🙃
Ex succinylcholine (a synthesized chemical known as the perfect poison for murder) Acetylcholine receptor antagonist (initial depolarization but then blocks receptor) Flaccid paralysis
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Neuromuscular junction drug 🥸
Neostigmine (synthesized chemical) Inhibits acetylcholinesterase activity Spastic paralysis
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Contractility 💪🏻 (drug)
Salbutamol (synthesized chemical aka albuterol) Enhances serca pump Activity Reduced contráctility
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Contráctility 👌
Caffeine (chemical found in seeds and nuts or leaves used as un insecticide by the plants) Enhances ca release at SR Increased contráctility
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Neuromuscular junction 🥴
Botulism Blocks snare protiens Flaccid paralysis
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Neuromuscular junction 🕷
Latrotoxin (black widow spider poison) Snare protien agonist Spastic paralysis