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VET200 SEM 1 > NEUROMUSCULAR > Flashcards

NEUROMUSCULAR Flashcards

1
Q

what is the somatic neuromuscular junction (NMJ)?

A
  • Synapse between motor neurons and skeletal muscle fibres
  • Controls muscle contraction (voluntary movement) - if motor axon fires an action potential then muscle will contract
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2
Q

process of synaptic transmission at NMJ

A
  1. AP in nerve terminal opens voltage-gated calcium channels
  2. Calcium influx triggers exocytosis of ACh filled synaptic vesicles
  3. ACh binds to nicotinic cholinergic receptors on muscle
  4. Na+ entry through nicotinic ACh receptors produces EPSP (EPP) (positive charge coming into cell = depolarising graded potential)
  5. EPSP depolarises voltage-gated sodium channels to threshold —> skeletal muscle action potential
  6. ACh degraded by acetylcholinesterase
    Called ‘nicotinic’ ACh receptors because nicotine is an agonist for the receptor
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2
Q

what NMJ features enable fine motor control

A
  1. Nicotinic ACh receptors are ionotrophic -> rapid depolarisation of muscle cell when transmitter binds -> very fast response/contraction
  2. EPSPs are Huge (lots of ACh released and high density of receptors = reliable AP firing in muscle
  3. enzymatic degradation of ACh quickly stops transmission = precise timing of muscle contractions
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3
Q

what are Nicotinic ACHRs?

A

ionotrophic receptors found a NMJ and autonomic ganglia

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4
Q

What are muscarinic AChRs?

A

metabotropic receptors found on autonomic target organs (cardiac muscle, smooth muscle, glands)

  • agonists increase muscle contraction, antagonists decrease
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5
Q

compare and contrast Botulism and Tetanus

A

BOTH: affect protein involved in synaptic vesicle exocytosis
BOTULISM:
- carcass of infecteed animal, canned food
- Flaccid paralysis, difficulty swallowing, respiratory failure
- blocks ACh release -> targets NMJ at PNS
- blocks process for contraction
TETANUS:
- Clostridium tetanii, anaerobic bacteria
- contaminated wound
- Blocks glycne/GABA release (neurotransmitter) -> targets inhibitory synapses in the CNS
- Targets Renshaw cells (inhibitory interneurons in spinal cord) a muscle contracture
- Stiff gait, pricked ears, risus sardonicus, clamped jaw, hypersensitivity to sound
- blocks inhibitory processes (GABA lessens ability of nerve cell to send signals -> usually would decrease contraction, but is inhibited by tetanus proteins) = increased contraction

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6
Q

Wha are the 8 possible effects of toxins in the NMJ:

A
  1. interference with acetylcholine release -> increase or decrease release of vesicles
  2. interference with acetylcholinesterase -> break it down = prolonged and constant muscle spasm
  3. potassium channel blockade = increased contraction due to increased action potentials
  4. calcium channel blockade = reduces exocytosis of ACh
  5. sodium channel activation = increased AP and contractions
  6. sodium channel blockade = decreased AP in muscle cells (post)
  7. nicotinic Ach receptor agonists = increase contraction (more sodium entry)
  8. nicotinic Ach receptor antagonists = decrease sodium entry and contractions
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7
Q

Identify each toxin as post or pre-synaptic:
1. batrachotoxin
2. tetrodotoxin
3. paradoxin (beta-neurotoxin)
4. holocyclotoxin
5. alpha-latrotoxin
6. anatoxin-a
7. cobratoxin (alpha-neurotoxin)
8. fasciculin

A
  1. BOTH
  2. BOTH
  3. PRE
  4. PRE
  5. PRE
  6. POST
  7. POST
  8. POST
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8
Q

what is the main effect of each of the follow (mechanism):
1. batrachotoxin
2. tetrodotoxin
3. paradoxin (beta-neurotoxin)
4. holocyclotoxin
5. alpha-latrotoxin
6. anatoxin-a
7. cobratoxin (alpha-neurotoxin)
8. fasciculin

A
  1. irreversibly binds to voltage-gated Na+ channeland activates permanently (opening) -> membrane permanently depolarised and inhibits NMJ
  2. voltage-gated Na+ channel blocked -> blocks action potentials
  3. blocks Ach vesicle release -> inhibitory at NMJ
  4. blocks voltage gated Ca2+ channels = prevents release of Ach vesicles -> inhibitory at NMJ
  5. increases Ca2+ permeability by creating pore permeable to Ca2+ = enhanced release of ACh vesicles = excitatory at NMJ
  6. nicotinic acetylocholine receptor agonist = opens ligand-gated sodium channel = excitatory at NMJ
  7. nAChR antagonist = blocks ligand-gated sodium channels = inhibitory
  8. anticholinesterase inhibitor -> muscle contraction can’t stop = excitatory
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9
Q

type of paralysis of each:
1. batrachotoxin
2. tetrodotoxin
3. paradoxin (beta-neurotoxin)
4. holocyclotoxin
5. alpha-latrotoxin
6. anatoxin-a
7. cobratoxin (alpha-neurotoxin)
8. fasciculin

A
  1. flaccid
  2. flaccid
  3. flaccid
  4. flaccid
  5. spastic
  6. spastic
  7. flaccid
  8. spastic
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10
Q

what do somatic and autonomic nervous systems control

A

somatic = skeletal muscle (voluntary)
autonomic = smooth and cardiac (mostly involuntary)

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11
Q

what are z-lines and M-lines of a sarcomere

A

z-line = ends of sarcomere, zi-zag, anchor actin flaments (thin)
m-lines - middle, anchor thick filamnets (myosin)

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12
Q

what is titin for?

A
  • muscle stability and relaxation
  • huge elastic molecule
  • connects M and Z line and keeps in place, can return to og position after contraction
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13
Q

what are troponin and tropomyosin?

A

troponin = Ca2+ binding protein
tropomyosn lies over actin filaments -> moved by myosin to expose myosin binding sites

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14
Q

what are the 4 major steps in muscle function?

A
  1. Excitation
    - Triggering of muscle action potential
  2. Excitation-contraction coupling
    - Imitation of contraction by the muscle action potential
  3. Contraction (cross bridge cycle)
    - Movement and/or force generation by muscle fibres
  4. Relaxation
    - Termination of movement and/or force generation by muscle fibres
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15
Q

what occurs during excitation

A
  • NMJ synaptic activation
  • EPP = end plate potential, special term for an EPSP at the neuromuscular junction
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16
Q

what occurs during Excitation-contraction coupling

A

Events between firing of a muscle Ap and start of contraction
1. Cholinergic transmission at NMJ —> AP firing in skeletal muscle cell
2. AP spreads along sarcolemma and down t-tubules (depolarisation transported deep into the muscle cell)
3. AP activates dihydropyrine receptors (voltage gated) which open ryanodine receptors (Ca2+ channels) on Sarco Retic
4. Ca2+ released from SR binds troponin, which displaces tropomyosin from myosin binding sites on actin molecules
5. Contracting (crossbridge cycling)

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17
Q

how is Ca2+ released from SR

A
  • AP in t-tubule
  • Changes shape of voltage-sensitive Ca2+ channels dihydropyridine receptors (DHPRs)
  • shape of DHPRs open voltage gated Ca2+ channels called ryanodine receptors (RyRs)
  • Ca2+ diffuses down concentration gradient from SR to cytoplasm
  • Initial release of Ca2+ from SR opens additional Ca2+ channels in SR (called calcium-induced calcium release)
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18
Q

when sarcomeres shorten, does the whole muscle shorten?

A

not always:
- depends on load on muscle
contracttion can cause:
1. shortening
2. tension (change in force)

19
Q

wha is isometric contraction?

A
  • heavy load
  • force generaed at peak of contraction less than load on muscle
  • Sarcomeres shorten but muscle length does not change (constant length, isometric)
  • Instead, muscle force production changes (increases)
20
Q

what is isotonic contraction

A
  • light load
  • Force generated at peak of contraction greater than load on muscle
  • Initially, same as isometric contraction (isotonic contractions have an isometric component)
  • Once force generated > load, muscle length changes (shortens) and force stays constant (constant force, isotonic)
21
Q

explain steps of cross bridge cycle

A
  1. Myosin binds to actin -> phosphate released
  2. power stroke -> myosin head pivots from cocked back position towards centre of sarcomere, pulls actin filaments towards centromere
  3. Rigor (actin and myosin tightly bound)
    - in between step 3 and 4, ATP binds to myosin head
  4. myosin detaches from actin
  5. cocking of myosin head – requires ATP hydrolysis to occur between step 4 and 5
22
Q

how is relaxation achieved

A
  • Cytoplasmic calcium concentration depends on balance between Ca2+ release from and Ca2+ reuptake to the SR
  • Elastic recoil of titan helps muscle return to resting length
  • During ongoing contraction increased Ca2+ concentration in cytosol causes closure of Ca2+ channels in SR, further limiting release
23
Q

what is a muscle twitch?

A

Mechanical response of muscle cell, motor cell, motor unit, or whole muscle to single action potential

24
wha is the latent period
delay between muscle AP firing and start of contraction
25
what effectts individual skeletal muscle fibre force
1. frequency of stimulation - repeated MPs release Ca2+ faster than can be taken up by SR = greater force. summation of twitches = greater force 2. fibre diameter - more sarcomeres in parallel = strength 3. resting muscle length - if muscle more stretched before contracts, then actin and myosin move further - more force - if too stretched, too far to reach so lose force
26
compare smooth muscle to skeletal muscle
smooth is slower, susained for longer and requires less energy per unit of force - no t-tubulkes - no straitions - gap junctions between cells (ions flow freely)
27
what is the trigger for smooth muscle contracton?
- Ca2+ elevation in muscle, NOT AP firing
28
explain exciation of smooth muscle
- Trigger for contraction is Ca2+ elevation, most often involving Ca2+ entry form the EXTRACELLULAR SPACE Via ligand, voltage or mechanically gated channels - Initiated by many different signals: 1. Spontaneous activity of pacemaker smooth muscle cells 2. Stretch of smooth muscle cells 3. Neutrally released transmitters 4. Circulating (hormones) or locally generated (paracrine) chemicals
29
explain Excitation-contraction coupling of smooth muscles
1. Ca2+ enters through gated ion channels 2. Ca2+ entry triggers Ca2+ release from SR 3. Ca2+ binds to calmodulin (CaM) Ca2+-CaM activates MLCK MLCK phosphorylates myosin light chains —> increased myosin ATPase activity Activated myosin starts cross bridge cycling
30
why is smooth muscle adapted for longer contraction
- Smooth muscle myosin thick filaments have no bare zone - can slide along actin for long distance -Smooth muscle myosin has slower rate of cross bridge cycling (—> slower contraction phase)
31
how does smooth muscle relax?:
1. Ca2+ pumped out of cell or into SR, decreasing cytoplasmic Ca2+ (calcium sodium pump also present, this goes against calciums conc gradient but because sodium is coming in it works out!) - Ca2+ unbinds from calmodulin (CaM) inactivating MLCK - Myosin phosphatase removes phosphate from myosin, decreasing myosin ATPase activity - Reduced myosin ATPase activity —> less cross bridge cycling *removing cytoplasmic Ca2+ is not enough, stays latched to smooth muscle so takes time to detach -> sustained contraction without fatigue
32
single unit vs multi unit smooth muscle
single: - gap junction coupling - few neurons - urogenital and gastroinestinal - oscillating RMP, phasic contractions (fast and breif) multi: - no gap junction coupling - rich nerve supply (autonomic) - in airways, blood vessels - steady RMP, tonic contractions (slow)
33
what is audtorhythmicity?
- generates own rhythm - Does not require input from the nervous system - Continues to beat for some time when removed from body
34
Types of cardiac muscle cells
1. Pacemaker cells - Concentrated in SA and AV nodes - Initiate APs by spontaneously generating pacemaker potentials - Initiate contraction, set heart rate 2. Conduction fibres - Seen in mammals for oxygen delivery to the brain - Bundle of His, Purkinje fibres - Large diameter muscle fibres - Specialised for rapid AP conduction (4m/sec vs <0.5 m/sec in myocardial cells) 3. Myocardial cells - Generate force - Majority of cardiac muscle cells
35
How are cardial muscle cells coupled?
Adjacent cardiac cells electrically and mechanically coupled at intercalated disks. These contain: 1. gap junctions -> electrical coupling, spread of APs 2. Desmosomes -> mechanical coupling, resistant to mechanical stress
36
Process of Excitation for cardiac muscle cells
- Trigger for contraction is myocardial cell AP firing - Trigger for myocardial cell AP firing is pacemaker cell AP firing - Control of cardiac muscle is myogenic (signal for contraction arises within heart muscle)
37
How do pacemaker cells generate APs??
- APs generated SPONTANEOUSLY, without external stimulation - RMP slowly depolarises to threshold, triggering an AP - Pacemaker potential = slow, spontaneous depolarisation to threshold
38
process of spontaneous AP firing in Pacemaker cells
1. ‘Funny’ Na+ channels open = Na+ influx, K+ channels close 2. Funny channels close , Voltage gated T-type Ca2+ channels open —> Ca2+ influx 3. Voltage gated L-type Ca2+ channels open —> Ca2+ influx 4. Voltage gated K+ channels open —> K+ efflux ② L-type Ca2+ channels close
39
explain electrical activity of myocardial cells
- No pacemaker activity - Depolarisation spreads from pacemaker cells (or other myocardial cells) - Very long AP - Very long refractory period Important to prevent tetanus of heart muscle
40
How are APs generated ionically in myocardial cells?
1. Voltage gated Na+ channels open —> Na+ influx 2. Na+ channels inactivate stops Na+ influx —> slight repolarisation 3. L-type Ca2+ channels open —> Ca2+ influx —> sustained depolarisation 4. Voltage gated K+ channels open (triggered in 2, but open slowly) —> K+ efflux —> repolarisation
41
why is cardiac muscle resistant to tetanus
- long refractory period (sustained depolarisation during plateu phase) - means that muscles have time to relax and fill heart chambers with blood before another contraction begins (second AP fired)
42
explain Excitation-contraction coupling of cardiac muscle
1. Current spreads to myocardial cell via gap junctions 2. AP travels along plasma membrane and down T-TUBULES 3. Voltage gated Ca2+ channels open —> Ca2+ entry 4. CA2+ INDUCED CA2+ RELEASE from SR via ryanodine receptors 5. Ca2+ binds to troponin, exposes myosin binding sites on actin 6. Crossbridge cycling (contraction)
43
How does relaxation of cardiac muscles occur?
1. Ca2+ dissociates from troponin 2. Ca2+ pumped into SR AND Ca2+ transported out of cell by Ca2+/Na+ exchanger driven by Na+ concentration gradient maintenance by Na+/K+ ATPase pump
44
what are sympathetic and parasympathetic branches for
- symp = fight or flight, emergency, stress, exercise - para = rest and digest, relaxed states
45
what are autonomic neuron systems made of
- two motor neuron system - Synapse is usually, but not always, in a ganglion - Presynaptic axon is (lightly) myelinated, postsynaptic is non-myelinated
46
differences between symp and parasympathetic systems
Symp: - Shorter presynaptic, longer postsynaptic axon - Ganglion is close to vertebrae, not target organ - Postsynaptic NT is noradrenaline (α, β) para: - Longer presynaptic, shorter postsynaptic axon - Ganglion is close to (or within wall of) target organ - Postsynaptic NT is acetylcholine (mAChR)

VET200 SEM 1 (4 decks)

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