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
Q

what does electron microscopy reveal

A

vesicle in the apparent act of exocytosis

26
Q

what does a black widow spider venom(alpha Latrotoxin, aka -a-LTX) do

A

it influences spontaneous transmitter release

27
Q

what is exocytosis

A

vesicle fusion

28
Q

what is endocytosis

A

recovery of vesicular membrane after fusion

29
Q

what would you expect to see on a mepp recording with a control and with the black widow venom

A

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
Q

what would happen after being bitten by the black widow venom

A

depletion of vesicles
inhibition of endocytosis
distended terminal
paralysis

31
Q

list the simplified model of fast synaptic transmission

A

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