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Question 1

What is a key feature of Ca channels?

Answer 1

Are very selective – will only let calcium through

Question 2

How do action potentials open calcium channels in cell membranes?

Answer 2

Depolarisation at the nerve terminal causes voltage gated Ca channels to open. Calcium enters the cell and causes the intracellular levels of Ca to increase. The increase in intracellular calcium levels causes neurotransmitters to be released.

Question 3

How do the levels of calcium differ from those of other ions in the cell membrane?

Answer 3

The intracellular concentration of calcium is so low that th inflow of Ca ions raise the levels significantly.

Question 4

Describe the structure of calcium channels

Answer 4

Four repeated subunits which wrap around to form an aqueous pore. Have numerous isoforms which are found in different locations throughout the body and have different blockers

Question 5

What is the most common calcium channel and what blocks it?

Answer 5

Alpha (1C,D,S) – type LFound in all muscles, neurones and in lungsBlocked by dihydropyridines e.g. Nifedipine

Question 6

What components make up a functional channel?

Answer 6

Pore forming subunit is needed for a functional channelOther subunits modify properties to allow for correct regulationE.g. Glycosylation and phosphorylation sites

Question 7

What process occurs to release neurotransmitters?

Answer 7

Exocytosis

Question 8

Describe the structure of the neuromuscular junction and give the neurotransmitter and what removes it

Answer 8

Has a short synaptic cleft to allow for rapid diffusionACh is broken down quickly by acetylcholinesterase – [ACh] is increased quickly, then removed quickly

Question 9

Describe the process of transmitter release.

Answer 9

Ca enters through voltage gate calcium channels Ca binds to synaptotagminVesicles are brought close to the membraneSnare complex changes conformation to make a fusion poreThe transmitter is released through the pore

Question 10

What assists in efficient transmission?

Answer 10

Ca channels are located close to the vesicles release sites so exocytosis will occur quickly

Question 11

What does binding of ACh to nicotinic receptors cause?

Answer 11

Binding of 2 ACh molecules causes nicotinic ACh rceptors to open. They are cationic channels –> aren’t very selective When ACh leave then channels closeThe channel produces a fast depolarisation due to Na gradient– it produces an end plate potential, which raises the mule above threshold to produce an action potential

Question 12

What do competitive blockers do?

Answer 12

Competitively block nicotinic ACh receptors by binding at the molecular recognition site

Question 13

Give the name of a competitive blocker and what it does

Answer 13

TubocurarineSits in receptor site but does not stimulate the opening of an ion channel or the binding of ACh – causes muscle paralysis

Question 14

Give the name of a depolarising blocker and how it blocks the receptor

Answer 14

Succinylcholine– causes a maintained depolarisation which fails to activate Na+ channels (are in inactivated state – accommodation) – opens the channels, but are desensitized

Question 15

What is the normal depolarisation mechanism of ACh binding?

Answer 15

A brief depolarisation will activate adjacent Na channels due to local spread of charge. This causes an action potential to be generated.

Question 16

What are miniature end plate potentials?

Answer 16

Small depolarizations which do not reach threshold– they correspond to spontaneous release of vesicles which measure at about 1 mV

Question 17

What is myasthenia gravis?What does it cause?

Answer 17

An autoimmune disease which targets nicotinic ACh receptors Sufferers have profound weakness which increase with exercise

Question 18

What causes myasthenia gravis?What happens to end plate potentials?

Answer 18

Causes by antibodies which are directed against nicotinic ACh receptors on the post synaptic membrane of skeletal muscle. They cause a decrease in the number of functional receptors due to:Complement mediated lysis and receptor degradation End plate potentials are reduced leading to muscle weakness and fatigue Less receptors are available which causes a smaller response

Question 19

Give a treatment for myasthenia gravis and how it helps

Answer 19

Acetylcholinesterase inhibitors– can improve the action potential conduction

Question 20

How do end plate potentials generate an action potential?

Answer 20

End plate potentials depolarise adjacent muscle membrane which activates voltage gated Na channels. This initiates an action potential in the muscle fibre which will contract due to excitation-contraction coupling

Question 21

Describe a nicotinic acetylcholine receptor, where it is found and what it generates.

Answer 21

It is a ligand gated ion channelFound in skeletal muscle and in preganglionic neuronesIt causes fast depolarisation

Question 22

Describe muscarinic ACh receptors

Answer 22

Have no ion channels – are g-protein coupled which causes a cascade of events inside the cell therefor giving a slower response than with nicotinic a receptors