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Physiology and Pharmacology > Synapses, neuromuscular junctions > Flashcards

Synapses, neuromuscular junctions Flashcards

1
Q

What is a neuromuscular junction?

A

Synpase between motor neurone and skeletal muscle fibre

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2
Q

Which ion channels are located in the neurone terminal?

A

Votage-gated sodium ion channels

Voltage-gated potassium ion channels

Voltage-gated calcium ion channels

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3
Q

What causes the voltage-gated calcium ion channels in the neurone terminal to open?

A

Incoming action potential causes neurone terminal to be depolarised

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4
Q

How do calcium ions move through the open voltage-gated calcium ion channels in the neurone terminal?

A

Move into the neurone terminal

down their concentration gradient

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5
Q

What do the influxed calcium ions in the neurone terminal do?

A

Bind to synaptotagmin

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6
Q

What does calcium-bound synaptotagmin in the neurone terminal do?

A

Brings vesicles containing neurotransmitter closer to the pre-synaptic membrane

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7
Q

What neurotransmitter do the vesicles in a neuromuscular junction contain?

A

Acetylcholine

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8
Q

What do the vesicles containing acetylcholine do when they’re near the pre-synaptic membrane?

A

Snare complex fuses the vesicle membrane and the pre-synaptic membrane together
acetylchole is released into synaptic cleft

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9
Q

What does acetylcholine in the synaptic cleft do?

A

Diffuses across synaptic cleft
binds to nicotinic acetylcholine receptors on the skeletal muscle membrane, 2 per receptor
causing it to open

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10
Q

What passes through open nicotinic acetylcholine receptors? What passes through most?

A

Sodium ions - more of these pass through

Potassium ions

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11
Q

Why do sodium ions largely pass through open nicotinic acetylcholine receptors compared to potassium ions?

A

Because there is greater driving force for sodium ions to enter the skeletal muscle fibre
since membrane potential is further away from ENa

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12
Q

What happens to the membrane potential of the skeletal muscle fibre due to influx of sodium ions?

A

Membrane potential depolarises
nearby voltage-sodium ion channels open
action potential is generated

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13
Q

What happens to acetylcholine bound to nicotinic acetylcholine receptors? What is the importance of this?

A

Broken down by acetylcholinesterase

Terminates the signal from motor neurone to skeletal muscle fibre
so don’t remain contracted

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14
Q

How does increasing the number of action potentials along the axon affect the neurone terminal?

A

Increased influx of calcium ions
more vesicles fuse with pre-synaptic membrane
more acetylcholine released

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15
Q

What is the structure of a voltage-gated calcium ion channel?

A

Single polypeptide chain, called alpha subunit
Four parts
Each part is made up of six transmembrane domains

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16
Q

What is the function of the fourth transmembrane domain in a voltage-gated calcium ion channel?

A

Voltage sensor

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17
Q

What is the significance of the fifth and sixth transmembrane domains in a voltage-gated calcium ion channel?

A

Between them is pore region

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18
Q

What is the signifiance of the third and fourth parts in a voltage-gated calcium ion channel?

A

Between them is inactivation particle

19
Q

Are voltage-gated sodium ion channels or calcium ion channels faster at activating and inactivating?

A

Voltage-gated sodium ion channels

20
Q

What causes the inactivation of voltage-gated calcium ion channels?

A

Calcium ions passing through them

giving increased concentration of intracellular calcium

21
Q

What are the types of blockers of nicotinic acetylcholine receptors?

A

Competitive blocker

Depolarising blocker

22
Q

What is an example of a competitive blocker of nicotinic acetylcholine receptors?

A

Curare

23
Q

How do competitive blockers of nicotinic acetylcholine receptors work?

A

Compete with acetylcholine for ligand-binding site on the nicotinic acetylcholine receptors
block the ligand-binding site
so acetylcholine can’t bind and nicotinic acetylcholine receptors can’t open

24
Q

How are the effects of competitive blockers of nicotinic acetylcholine receptors overcome?

A

By increased concentration of acetylcholine

25
Q

What is an example of a depolarising blocker of nicotinic acetylcholine receptors?

A

Succinylcholine

26
Q

How do depolarising blockers of nicotinic acetylcholine receptors work?

A

Bind to nicotinic acetylcholine receptors and cause them to open
not broken down well by acetylcholinesterase
depolarisation is maintained
voltage-gated sodium ion channels inactivate and do not reactivate due to lack of hyperpolarisation

27
Q

How do blockers of nicotinic acetylcholine receptors affect muscle contraction?

A

Muscles don’t contract, are paralysed

28
Q

What is the pathophysiology of myasthenia gravis?

A

Autoantibodies against nicotinic acetylcholine receptors
are destroyed
skeletal muscle fibre membrane doesn’t reach threshold
action potential not generated
muscle doesn’t contract

29
Q

What are the symptoms of myasthenia gravis?

A

Muscle weakness

Muscle fatigue

30
Q

What exacerbates the symptoms of myasthenia gravis?

A

Exercise

31
Q

What do synapses occur between?

A

Neurone to neurone

Neurone to muscle fibre

Neurone to gland cell

Sensory cell to neurone

32
Q

What are the types of synapses?

A

Fast

Slow

33
Q

What is a fast synapse?

A

Neurotransmitter binds to receptor on post-synaptic membrane
which is a ligand-gated ion channel
causing it to open
and allowing ions to pass through

34
Q

What are the types of fast synapses?

A

Excitatory

Inhibitory

35
Q

What are excitatory fast synapses?

A

The ligated-gated ion channel that opens is for sodium ions or calcium ions, whose influx gives membrane depolarisation

36
Q

What is the name of the depolarisation caused by excitatory fast synapses?

A

Excitatory post-synaptic potentials

37
Q

What are inhibitory fast synapses?

A

The ligand-gated ion channel that opens is for potassium or chloride ions
whose movement across the post-synaptic membrane gives hyperpolarisation

38
Q

What is the name of the hyperpolarisation caused by inhibitory fast synapses?

A

Inhibitory post-synaptic potential

39
Q

Are excitatory/inhibitory post-synaptic potentials the same as action potentials?

A

No

40
Q

How are excitatory/inhibitory post-synaptic potentials different to action potentials?

A

They are graded, meaning their strength varies

They last for longer than an action potential

41
Q

How are excitatory/inhibitory post-synaptic potentials graded?

A

Based on amount of neurotransmitter binding to receptors on post-synaptic membrane
based on number of vesicles fusing with pre-synaptic membrane
based on calcium ion influx
based on frequency of incoming action potentials into pre-synaptic neurone terminal

42
Q

What are slow synapses?

A

Neurotransmitter binds to receptors on post-synaptic membrane
signal transduction occurs to open ion channel, which is a separate protein

43
Q

What are the types of mechanisms by which slow synapses work?

A

Neurotransmitter binds to GPCR
activated G-protein itself binds to ion channel and opens it up

Neurotransmitter binds to GPCR
signalling cascade
effector protein binds to ion channel and opens it up

44
Q

Which mechanism of slow synapses is faster? Why?

A

Where the activated G-protein itself binds to ion channel and opens it up
because it’s more localised

Physiology and Pharmacology (20 decks)

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