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Physiology > The Neuromuscular Junction > Flashcards

The Neuromuscular Junction Flashcards

0
Q

What are the two types of synapes?

A

1) Electrical and 2) Chemical

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1
Q

What is a synaptic delay?

A

the time between arrival of an action potential in the presynaptic neuron and a potential change in the post synaptic cell

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2
Q

What are properties of electrical synapses?

A
  • direct passage of current from one cell to another cell
  • small synaptic cleft (20A)
  • pre and post synaptic cells connected by gap junctions
  • no synaptic delay
  • pre and post synaptic elements are equal in size
  • bidirectional transmission
  • uncommon in mammalian CNS or PNS
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3
Q

What are properties of chemical synapses?

A
  • uses chemical neurotransmitters in vesicles in presynaptic (preSyn) ending
  • large synaptic cleft (several hundred A)
  • no electrical connection between elements
  • presence of synaptic delay
  • preSyn is much smaller than postSyn cell
  • postSyn cell has neurotransmitter receptors
  • Mostly UNIdrectional transmission
  • Most common type of synapse in CNS and PNS
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4
Q

What is a neuromuscular junction? What are other names for it?

A

the synapse between a motor neuron and a skeeltal muscle fiber

Also known as myoneural junction && end plate

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5
Q

Describe the structure of the NMJ.

A

Presynaptic end has clear vesicles with acetylcholine (ACh) neurotransmitter. The vesicles line release sites called active zones.

The synaptic cleft is approx 500A (huge!).

On the PostSyn membrane, junctional folds contain ACh receptors on peaks. The peaks line up with active zones. Also on the membrane are acetylcholinesterase (AChE), which degrades ACh.

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6
Q

Describe the sequence of events during neuromuscular transmission.

A
  1. Action potential reaches presynaptic ending
  2. Depolarization opens voltage gated Ca channels on active zone.
  3. Ca2+ influx (rushes in)
  4. Ca2+ causes synaptic vesicles to fuse with plasma membrane and release ACh via exocytosis
  5. ACh diffuses across synaptic cleft and combines with ACh receptors on PostSyn membrane
  6. ACh + receptor cause monovalent cation channels to open, resulting in a depolarization called the end plate potential.
  7. Muscle membrane surrounding the end plate becomes depolarized, opening Na+ voltage-gated channels in the muscle membrane, which causes an AP to propagate in both directions away from the end plate.
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7
Q

What is the Reversal Potential? What happens if it increases permeability for one ion? multiple ions?

A

The membrane potential at which there is no net current due to the action of the transmitter

If 1 ion’s permeability is increased. Reversal potential (RP) = equilibrium of that potential.
>1 ion permeability is increased, RP = in between the equilibrium potential of the ions involved

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8
Q

In the absence of nerve stimulation, what are small depolarizations that occur at the NMJ called?

A

Miniature end-plate potentials (MEPP)

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9
Q

What is the size of an End Plate Potential dependent on?

A

Extracellular Ca2+ concentration.

[Ca2+]_o

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10
Q

Describe the relationship between extracellular Ca2+ concentration and EPP.

A

As the [Ca2+]_o is reduced, EPP becomes smaller until it becomes nothing under nerve stimulation.

The smallest EPP is the miniature end-plate potentials (MEPPs).

The size of the EPP under low extracellular Ca2+ concentrations fluctuates but is always some integral multiple of the MEPP.

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11
Q

EPPs are made up of multiples of a _________ amount.

A

quantal

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12
Q

What are properties of Transmitter Release at the NMJ?

A
  • Each quantum transmitter has thousands of molecules of ACh
  • An Action Potential releases hundreds of quanta
  • Amount of transmitter released is far in excess of what is actually necessary to produce an Action potential.
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13
Q

Where and from what is ACh synthesized?

A

ACh is synthesized in the nerve terminal from dietary choline and acetylCoA

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14
Q

What transports ACh into vescles?

A

specific ACh transport proteins in the vesicle membrane

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15
Q

Describe the release of stored ACh.

A
  • Released in quantal packets (1 vesicle = 1 quanta)
  • 10,000 molecules of ACH per vesicle
  • Sometimes spontaneously released by PreSyn, resulting in MEPP (usually <1mV in amplitude)
  • When released by AP, hundreds of vesicles are leased resulting in an EPP strong enough to trigger an action potential
16
Q

What molecules stops ACh at the NMJ? How does it stop ACh?

A

Acetylcholinesterase (AChE) hydrolyzes Ach into acetate and choline.

17
Q

How do cholinesterase inhibitors work?

A

cholinesterase inhibitors prevent the hydrolysis of ACh, thus prolonging the action of ACh

18
Q

What disorders affect the NMJ?

A

Myasthenia Gravis
and
Lambert-Eaton Syndrome

19
Q

What is Myasthenia Gravis? What are symptoms? What drugs are used to treat it?

A

an autoimmune disorder where antibodies are produced against nicotinic ACh receptors. The nerve terminals are normal but ACh receptors are sparse and junctional folds are shallow

Forms of the disease include weakness in only extraocular muscles and weakness of all skeletal muscles as the day progresses

Drug treatment involves use of cholinesterase inhibitors.

20
Q

What is Lambert-Eaton syndrome? What are symptoms?

A

In Lambert-Eaton syndrome, patients have antibodies against the voltage-gated Ca2+ channels in nerve terminals. This reduces Ca2+ influx, reducing transmitter release.

Symptoms include weakness in primarily limb musculature, not ocular muscles.

50% of patients have small cell lung carcinoma. Appearing 3 years before lung cancer, Lambert-Eaton syndrome is useful in detecting the cancer at an early stage.

21
Q

What types of toxins and Drugs affect synaptic transmission?

A

1) Those that affect the presynaptic action potential
2) Bacterial toxins
3) Agonists and antagonist of nicotinic ACh receptor
4) Inhibitors of AChE

22
Q

What are TTX and STX?

A

These are presynaptic Na channel blockers that prevent the action potential and inhibit ACh release

23
Q

What do tetraethylamonium (TEA) and dendrotoxin do?

A

These are presynaptic K+ channel blockers that slow repolarization and enhance ACh release by allowing greater Ca influx

24
Q

How does omega-conotoxin and divalent cations affect NMJ?

A

These are presynaptic Ca channel blockers inhibit Ca2+ influx, inhibiting release of ACh.

25
Q

What is the cause of botulism?

A

Botulinum toxin inhibits transmitter release from cholingergic endings by entering nerve endings and cleaving proteins related to vesicle fusion and exocytosis

26
Q

What is the cause of lockjaw?

A

Tetanus toxin inhibits transmittter release from inhibitory neurons in the spinal cord that normally inhibit muscle contraction by inhibiting alpha-motorneurons. The toxin enter peripheral nerves, travels to the spinal cord, and ends up in the inhibitory interneuron, where it inhibits the transmitter Glycine by cleaving proteins related to vesicle fusion and exocytosis.

27
Q

Which can can block synaptic transmission? Agonists or Antagonists of nicotine receptor

A

Both!

28
Q

Name some agonists and antagonists of nicotinic ACh receptor.

A

Agonist: carbamylcholine and succinylcholine
Antagonist: d-Tubocurarine (cuare)

Both produce flaccid paralysis. Agonists activate ACh reecptor, resistant to hydrolysis and by prolonging opening of ACh channels cause them to desensitize. Antagonists are competitive inhibitors of ACh, reducing the number of receptors available to bind ACh, thus reducing the amplitude of the EPP to sub threshold levels.

29
Q

What do inhibitors of AChE do? What are some examples of AChE inhibitors?

A

The inhibitors here amplify the end plate potential.

Examples include physostigmine or neostigmine (reversible inhibitors of AChE), oragnophosphorous compounds irreversible inhibitors of AChE), and anatoxin-a

30
Q

What are two reversible inhibitors of AChE? What do they do?

A

physostigmine and neostigmine

These inhibit AChE, resulting in prolonged duration and increased amplitude of EPP. These agents are slowly hydrolyzed and eventually lose effectiveness

31
Q

What does Sarin do?

A

Sarin is an organophosphorous compound, an irreversible inhibitor of AChe that blockade depolarization

33
Q

What is anatoxin-a?

A

As a organophosphorous neurotoxin from cyanobacteria, anatoxin-a is a inhibitor of AChE that amplifies the end plate potential and is responsible for poisoning of animals that drink from contaminated ponds.

Physiology (9 decks)

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