Synapses, neuromuscular junctions

Question 1

What is a neuromuscular junction?

Answer 1

Synpase between motor neurone and skeletal muscle fibre

Question 2

Which ion channels are located in the neurone terminal?

Answer 2

Votage-gated sodium ion channels

Voltage-gated potassium ion channels

Voltage-gated calcium ion channels

Question 3

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

Answer 3

Incoming action potential causes neurone terminal to be depolarised

Question 4

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

Answer 4

Move into the neurone terminal

down their concentration gradient

Question 5

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

Answer 5

Bind to synaptotagmin

Question 6

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

Answer 6

Brings vesicles containing neurotransmitter closer to the pre-synaptic membrane

Question 7

What neurotransmitter do the vesicles in a neuromuscular junction contain?

Answer 7

Acetylcholine

Question 8

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

Answer 8

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

Question 9

What does acetylcholine in the synaptic cleft do?

Answer 9

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

Question 10

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

Answer 10

Sodium ions - more of these pass through

Potassium ions

Question 11

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

Answer 11

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

Question 12

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

Answer 12

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

Question 13

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

Answer 13

Broken down by acetylcholinesterase

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

Question 14

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

Answer 14

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

Question 15

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

Answer 15

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

Question 16

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

Answer 16

Voltage sensor

Question 17

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

Answer 17

Between them is pore region

Question 18

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

Answer 18

Between them is inactivation particle

Question 19

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

Answer 19

Voltage-gated sodium ion channels

Question 20

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

Answer 20

Calcium ions passing through them

giving increased concentration of intracellular calcium

Question 21

What are the types of blockers of nicotinic acetylcholine receptors?

Answer 21

Competitive blocker

Depolarising blocker

Question 22

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

Answer 22

Curare

Question 23

How do competitive blockers of nicotinic acetylcholine receptors work?

Answer 23

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

Question 24

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

Answer 24

By increased concentration of acetylcholine

Question 25

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

Answer 25

Succinylcholine

Question 26

How do depolarising blockers of nicotinic acetylcholine receptors work?

Answer 26

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

Question 27

How do blockers of nicotinic acetylcholine receptors affect muscle contraction?

Answer 27

Muscles don't contract, are paralysed

Question 28

What is the pathophysiology of myasthenia gravis?

Answer 28

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

Question 29

What are the symptoms of myasthenia gravis?

Answer 29

Muscle weakness Muscle fatigue

Question 30

What exacerbates the symptoms of myasthenia gravis?

Answer 30

Exercise

Question 31

What do synapses occur between?

Answer 31

Neurone to neurone Neurone to muscle fibre Neurone to gland cell Sensory cell to neurone

Question 32

What are the types of synapses?

Answer 32

Fast Slow

Question 33

What is a fast synapse?

Answer 33

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

Question 34

What are the types of fast synapses?

Answer 34

Excitatory Inhibitory

Question 35

What are excitatory fast synapses?

Answer 35

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

Question 36

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

Answer 36

Excitatory post-synaptic potentials

Question 37

What are inhibitory fast synapses?

Answer 37

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

Question 38

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

Answer 38

Inhibitory post-synaptic potential

Question 39

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

Answer 39

No

Question 40

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

Answer 40

They are graded, meaning their strength varies They last for longer than an action potential

Question 41

How are excitatory/inhibitory post-synaptic potentials graded?

Answer 41

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

Question 42

What are slow synapses?

Answer 42

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

Question 43

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

Answer 43

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

Question 44

Which mechanism of slow synapses is faster? Why?

Answer 44

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