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BPK 306 > Neuromuscular Junction > Flashcards

Neuromuscular Junction Flashcards

1
Q

Components Neuromuscular Junction

A

Lower motor neuron
Muscle fibre

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2
Q

Regions of NMJ

A

Presynaptic region
Synaptic cleft
Postsynaptic region

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3
Q

What is a motor unit

A

One motor neuron, axon, presynaptic termini, muscle fibres

One motor neuron and all the fibres it innervates

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4
Q

What is the innervation ratio

A

Number of muscle fibres supplied by one motor neuron

Large innervation ratio- large motor unit

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5
Q

How are motor units recruited

A

As needed- small first
- diff threshold activation

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6
Q

Steps for action potential propagation between neurons

A
  1. Neurotransmitter synthesized and packaged into vesicles
  2. Action potential arrives at presynaptic terminal
  3. Voltage gated Ca channels open. Ca enters
    4.rise in Ca triggers fusion of synaptic vesicles with the presynaptic membrane
  4. Neurotransmitter diffuse across synaptic cleft and bind to specific receptors on postsynaptic cell
  5. Bound receptors activate postsynaptic cell
    7.neurotransmitter breaks down, is taken back up by presynaptic terminal or other cells, or diffuses away from the synapse

Note: axon terminus unmyelinated

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7
Q

Function presynaptic termini

A

Synthesis, storage and release of ACh
Stored in synaptic vesicles

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8
Q

How is ACh made

A

Choline and acetyl-CoA
Enzyme: choline acetyltransferase (ChAT)

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9
Q

How much ACh can one vesicle store

A

Quantum 6,000-10,000
“quantal release of ACh”

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10
Q

Where are vesicles stored

A

Immediate or secondary storage areas

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11
Q

What type of Ca channel is on presynaptic membrane

A

P-type Ca channel

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12
Q

Where can vesicles fuse (dock) at presynaptic membrane

A

Specific sites called active zones

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13
Q

What steps must happens to vesicle before fusion with presynaptic memrbane

A

Primed, Cocked, armed
Involves 25 proteins

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14
Q

What is the kiss and run mechanism

A

Recycles vesicles for reloading and reuse
Kiss- slight connection
Run- back into presynaptic neuron. Vesicle doesnt become part of membrane stays whole

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15
Q

What compounds are used in the docking phase of synaptic release and what is their function

A

v-SNARE= synaptobrevin
t-SNARES= syntaxin, SNAP-25
Form a zippered complex bringing the vesicle and target into proximity

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16
Q

What primes the complex after docked stage

A

Complexin

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17
Q

Explain the details of kiss phase

A

Ca enters and binds to synaptotagmin
Ca-synaptotagmin displaces complexin and binds the SNARE complex causing pore formstion (kiss) followed by release

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18
Q

Role of v-SNARES and t-SNARES with synaptic release

A

Form zippered complex bringing vesicle and target close together

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19
Q

Role of synaptotagmin

A

Ca binds to it. Together displace complexin and bind to SNARE complex causing pore formation

20
Q

Explain details of run phase

A

Ca depletes causing synaptotagmin to dissociate from SNARE complex
SNARE complex disassembles
Vesicle endocytoses (run) back into neuron

21
Q

What does tetanus toxin do and cause

A

Cleaves synaptobrevin
Causes rigid paralysis by blocking GABA (fn- inhibit neuronal transmission- reduce excitability) release
(TNTX)

22
Q

What does Botulism toxin do and cause

A

Cleaves synaptobrevin at NMJ (therefore no ACh release)
Causes flaccid paralysis- no contraction at all
(BTX)

23
Q

How is Ca removed from pre synaptic neuron after synaptic release

A

Extrusion by plasma membrane Ca ATP-ase (PMCA) and uptake by mitochondria

24
Q

Name the post synaptic receptor and what binds to it

A

Nicotinic acetylcholine receptor (NAChR)- transmembrane protein
2 ACh bind

25
Q

Name subunits of NAChR

A

2 alpha, 1B, 1 delta, 1 epsilon
Heteromeric pentamer

26
Q

What ions move through NAChR

A

Na move down electrochemical gradient

27
Q

When ___ moves through the NAChR it produces a ___

A

Na
Passive end plate potential (EPP) (graded/passive)

28
Q

What type of channel is NAChR

A

GPCR- ligand gated channel (ligand- ACh)

29
Q

Name types of ion channels in muscle (postsynaptic structure)

A

AChR
Na channel (voltage gated)
Cl- channel
K channel
Ca channel (not as channel but important- DHP mechanically coupled)

30
Q

What are mEPPs and when do they occur

A

Miniature end plate potentials
Occur spontaneously at motor end plate- due to spontaneous release of vesicles (ACh) without action potentials
Normal occuramce doesn’t lead to AP
mEPPs are additive

31
Q

What did the discovery of EPPs allow for

A

Determine quantal basis of synaptic release at NMJ

32
Q

What allows Ca to enter pre synaptic neuron

A

Increase in intracellular permeability to Ca
Enter via voltage gated Ca channels

33
Q

What causes EPP and what does it do

A

Increased permeability of Na and K
EPP depolarizes areas of muscle membrane adjacent to end plate - this initiates AP in muscle

34
Q

What can inhibit neuronal Na channels

A

Tetrodotoxin (puffer fish)= loss of sensation, paralysis of voluntary muscles, respiratory failure
Saxitoxin (algae- shellfish) tingling/burning, shortness of breath

35
Q

What inhibits K channels
What does this compound enhance

A

Dendrotoxin (snake)
Enhances ACh release, muscle hyperexcitability, convulsions

36
Q

What inhibits ACh release
What does it cause

A

Tetanus toxin (rigid paralysis)
Botulinum toxin (flaccid paralysis)

37
Q

What inhibits acetylcholinesterase

A

Physostigmine
DFP

38
Q

What inhibits AChR channel
What does it cause

A

D-tubocurarine
Alpha- bungarotoxin (snake) = paralysis, respiratory failure, death at high doses

39
Q

What compounds activate AChR channel

A

Nicotine
ACh (acetylcholine)

40
Q

What inhibits muscle Na channel

A

Tetrodotoxin
Saxitoxin (algae- paralytic shellfish poisoning) = tingling/ burning, shortness of breath
U-conotoxin

41
Q

What inhibits Ca channels

A

w-conotoxin

42
Q

What is myasthynia gravis and what does it target

A

Autoimmune disease targets postsynaptic NMJ= motor end plate (degenerates)

43
Q

What does myasthynia gravis cause in the body, symptoms, treatments

A

Causes Substantial loss of junctional folds- reduced number of NAChR
Symptoms impaired neuromuscular transmission, weakness of facial and body muscles
Treatments- acetylcholinesterase inhibitors (keep ACh around longer), immunosuppressants

44
Q

Symptoms of individual who has a neuromuscular transmission disorder

A

Weakness of cranial and skeletal muscles

45
Q

Clinical manifestations of myasthenia gravis

A

Diplopia- double vision
Ptosis- drooping upper eyelid
Weakness of facial, bulbar, respiratory, proximal limb muscles

BPK 306 (18 decks)

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