Week 13 lectures 1-3 skeletal neuro muscular junction Flashcards

1
Q

how fast can action potentials travel

A

120 metres/sec

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2
Q

how many neurons does the human brain have

A

100 billion

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3
Q

what is needed to open up vesicles

A

calcium ions , action potential

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4
Q

what is the neuromuscular junction

A

the synapse between a neurone and a skeletal muscle fibre

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5
Q

how many steps are involved in the release of a transmitter and what are they and how can they be influenced

A

there are 5 steps
Synthesis
storage
release
activation
inactivation
They are influenced by drugs and toxins resulting in resulting in either an increase or a decrease of transmission

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6
Q

how can drugs enhance synaptic transmission and explain

A

1) direct stimulation of the post-synaptic receptors by
a) the natural transmitter
b) analogues
2) indirect action via:
a) increased transmitter release
b) inhibition of transmitter removal

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7
Q

how can drugs inhibit synaptic transmission and explain

A

1)blocking synthesis, storage, or release from the presynaptic neuron.
2) Blocking post synaptic receptors

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8
Q

what are the names of drugs that directly act on receptors

A

agonists and antagonists

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9
Q

what are agonists and describe them entirely

A

agonists are drugs, hormones, or transmitters which can bind to specific receptors and initiate a conformational change in the receptor resulting in a biological response.

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10
Q

what are the two important properties of agonists and describe them

A

affinity (the ability of agonists to bind to receptors) and

efficacy (the ability of an agonist, once bound to a receptor, to initiate a biological response.

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11
Q

what is an antagonist

A

antagonists bind to receptors but do not activate them

They posses affinity but not efficacy

they block receptors activation by the agonists

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12
Q

what is a competitive antagonist

A

it competes with the agonist for the “agonists binding site” on the receptor.

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13
Q

what is the neurotransmitter at the neuromuscular junction (NMJ)

A

acetylcholine

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14
Q

how are synapses classified

A

according to the transmitter released from the presynaptic neurone

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15
Q

what does it mean if the transmission is cholinergic

A

the presynaptic neuron synthesises and releases acetylcholine (ACh)

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16
Q

What are the 2 classes of cholinoceptors and describe them

A

1) Nicotinic cholinoceptors (activated by ACh or the tobacco alkaloid nicotine but not the muscarine.

2) Muscarinic cholinoceptors activated by ACh or the fungal alkaloid muscarine but not nicotine

17
Q

how is fast transmission mediated

A

transmitter-gated ion channels

18
Q

how many subunits are there

A

5
beta
gamma
delta
2 alpha

19
Q

what flows throw the subunits into the cell

A

sodium ion cations flow in and potassium out

20
Q

what happens when an agonist binds to the receptor

A

induces a rapid conformational change to open the channel

21
Q

how quick can signalling happen

A

milliseconds

22
Q

what does mepps stand for

A

Miniature end plate potentials

23
Q

what happens when ACh is released from a single vesicle

A

many nicotinic ACh receptors are activated

24
Q

what happens when the ACh receptors are activated

A

the associated cation channels open and the Na+ ions flux into the muscle fibre to cause a local depolarisation at the endplate region (ie. a mepp)

25
what does electron microscopy reveal
vesicle in the apparent act of exocytosis
26
what does a black widow spider venom(alpha Latrotoxin, aka -a-LTX) do
it influences spontaneous transmitter release
27
what is exocytosis
vesicle fusion
28
what is endocytosis
recovery of vesicular membrane after fusion
29
what would you expect to see on a mepp recording with a control and with the black widow venom
control: miniature spikes as the transmitter is being released as normal venom: massive releases in the ACh neurotransmitter causing muscle spasms and massive spikes in the mepp recording
30
what would happen after being bitten by the black widow venom
depletion of vesicles inhibition of endocytosis distended terminal paralysis
31
list the simplified model of fast synaptic transmission
1) Presynaptic action potential 2) A synchronous Ca2+ influx via voltage-gated Ca2+ channels 3) Many vesicles undergo exocytosis releasing a large cloud of acetylcholine 4) Activation of many nicotinic acetylcholine receptors 5) This causes a large depolarization of endplate region of muscle cell (an epp) 6) If the depolarization is large enough it activates postsynaptic voltage-gated sodium channels to initiate an action potential