lecture 4: action potentials and synaptic transmission

Question 1

what is meant by the term ‘action potential’?

Answer 1

a rapid change in the membrane potential

Question 2

what was found in experiments to support the idea that the upstroke of the action potential is due to an increase in permeability to [Na+]?

Answer 2

reduced current in the presence of decreased [Na+]

Question 3

which type of feedback mechanism controls action potential initiation?

Answer 3

positive feedback loop

Question 4

what are the reasons why the Na/K pump cannot be involved in the repolarisation of the membrane?

Answer 4

• the amount of ions which move is too small to require this pump to re-establish resting concentration
• this pump would cause hyperpolarisation due to greater K+ efflux

Question 5

what is the difference between absolute refractory period and relative refractory period?

Answer 5

during ARP, all Na+ channels are closed. during RRP, the channels are recovering and an action potential can be initiated in the presence of a large enough stimulus

Question 6

describe the structure of a voltage-gated Na+ channel

Answer 6

-pore region -voltage sensor -inactivation particle
made from an alpha subunit with four similar repeats. the fourth region has many positively charged AAs which detect changes in membrane potential

Question 7

describe the structure of a voltage-gated K+ channel

Answer 7

-voltage sensing S4 region -pore region contributing to selectivity -4x a-subunits

Question 8

what does the propagation of the action potential along the axon rely on?

Answer 8

local current spread

Question 9

what is the neuromuscular junction?

Answer 9

a chemical synapse between a nerve and skeletal muscle fibre

Question 10

why is the nerve terminal so dense in Ca2+ channels?

Answer 10

Ca2+ influx is crucial for triggering exocytosis of neurotransmitters from the nerve terminal

Question 11

how is a neurotransmitter released?

Answer 11

1) AP arrives 2) voltage-gated calcium channels open 3) Ca2+ enters 4) Ca2+ promotes the release of neurotransmitter in vesicles

Question 12

why is it that Ba2+ can flow through a voltage-gated Ca2+ channel but not inactivate it?

Answer 12

inactivation of Ca2+ channels is dependent on Ca2+

Question 13

what is meant by ‘motor end plate’?

Answer 13

the neuromuscular junction of a skeletal muscle fibre, where the axon connects with the muscle fibre

Question 14

which key enzyme is located at the motor end plate in high concentrations?

Answer 14

Acetylcholine Esterase

Question 15

where are acetylcholine receptors found in skeletal muscle?

Answer 15

muscle membrane

Question 16

describe the process which leads to release of neurotransmitter (ACh) in skeletal muscle

Answer 16

1) Ca2+ entry via Ca2+ channels
2) Ca2+ binds to synaptotagmin, activating it
3) synaptotagmin brings the vesicle close to the membrane
4) snare complex makes a fusion pore; creating a pathway between vesicle and synaptic cleft
5) transmitter released through the pore

Question 17

how does release of acetylcholine trigger depolarisation of the muscle?

Answer 17

1) nAChR activated by ACh; when 2x ACh are bound, there is a conformational change resulting in influx of Na+
2) muscle membrane becomes depolarised

Question 18

describe the structure of the nicotinic acetylcholine receptor?

Answer 18

• 5 subunits

- ACh binds to each a-subunit, causing a conformational change resulting in the pore opening

Question 19

how does T-tubocurarine block depolarisation?

Answer 19

competitive block that sits in the ACh binding site without activating it, can be overcome in high concentrations of ACh

Question 20

How does succinylcholine cause a neuromuscular block?

Answer 20

activates ACh receptors but is not broken down by AChE, this means that maintained depolarisation causes the Na+ channels to inactivate