Block 2 100312 Neuromuscular Junction

Front 1

What are the sequence of events in neuromuscular transmission?

Back 1

1. AP-Nerve impulse depolarizes nerve terminal
2. Ca++ channels open and Ca++ flow in the cell
3. Ca++ cause vesicles containing Ach to exocytosis and sends Ach into synapse
4. Ach binds to receptors on post synaptic membrane of muscle cell
5. Binding of ACh receptors opens cation channels (Na+, K+)
6. Depolarization of muscle membrane (end plate potential)
7.AP in muscle cell
8. Ach is degraded in synapse by acetylcholinestrase

Front 2

Describe the structure of the nicotinic Ach receptor. Muscle vs brain receptors?

Back 2

-multimeric (5 subunits 2as, b, g d for muscle, only alpha and beta for brain)
- Ach binds to alpha subunit
- ligand gated ion channel
- after Ach binds, conformation change that allows Na+ and K+ to move down their conc. gradient

Front 3

What is the "active zone" of neuromuscular junctions?

Back 3

region of conventrated synaptic vesicles closest to the presynaptic membrane directly opposite the postynaptic folding

Front 4

How is Ach synthesized and broken down?

Back 4

Motor neuron synthesizes choline acetyltransferase that does: acetyl CoA + choline = Ach
Postsynaptic muscle cell synthesizes actylechoinesterase that hydrolizes Ach to acetate + choline

Front 5

What does curare and nicotine do to Ach receptors?

Back 5

curare= blocks Ach so relaxes muscle
nicotine= activates the receptors

Front 6

How is choline recycled in the synaptic cleft?

Back 6

High affinity transporters that are Na+ dependent takes up choline in the nerve terminal

Front 7

What do the drugs eserine (physostigmine) and neostigmine that are anticholinesterases do to muscle cells?

Back 7

enhance muscle contraction by inhibiting the action of Ach-esterase but if present for too long the muscle experience tetanus and becomes desensitized and un-responsive

Front 8

What causes the spike at the end plate potential?

Back 8

Na+ rushing in and K+ rushing out

Front 9

Is the end plate potential the consequence of active or passive properties of the muscle membrane? What does the epp look liek further from the end plate? What does that say about the resistance and capacitance?

Back 9

passive

response declines further from the end plate

Lower resistance

Front 10

What kind of drug is good to treat botulism (too little Ach released) or Myasthena Gravis (reduction of Ach receptors) and why?

Back 10

anticholinesterase, doesn't allows for the break down of Ach so it stays long and creates a longer response

Front 11

What are miniature EPPs?

Back 11

a vesicle of Ach is released without an AP which causes passive slight depolarization and causes a synchronized increase in the number of synaptic vesicles which disgorge their contents into the synaptic cleft to increase the number of channels opened to ensure

Front 12

What are the effects of hypercalcemia and hypocalcemia?

Back 12

Normal changes in Ca++ doesnt effect Ach release but hypercalcemia makes muscle membranes less excitable and blocks Na+ entry (muscle weakness) and hypocalcemia makes muscle more hyperexcitable and spontaneously twitching = hypocalcaemic tetany

Front 13

What are the effects of tetanus toxin?

Back 13

Blocks the release of inhibitory neurotransmitters (GABA, glycine) leading to enhanced excitation of motor neuro and spasms

Front 14

WHat are the effects of diptheria toxin?

Back 14

attacks schwann cells and causes demyelination

Front 15

What are the effects of tetrodotoxin?

Back 15

Blocks voltage dependent Na+ channelswhich causes paralysis since nerve transmission is blocked

Front 16

What are the effects of botulinum?

Back 16

prevents Ach containing vesicles from fusing to the membrane to produce paralysis

Front 17

If i was bitten by a black widow spider, what would happen

Back 17

promotes fusion of Ach vesicles that results in muscle tetany and spasms

Front 18

What does a-bungarotoxin do?

Back 18

binds to Ach receptors thus preventing muscle contraction