Pharmacology of the ANS and NMJ Flashcards Preview

Science For Med A ellen > Pharmacology of the ANS and NMJ > Flashcards

Flashcards in Pharmacology of the ANS and NMJ Deck (12):
1

What type of receptors are cholinergic nicotinic receptors?

Ionotropic

2

What type of receptors are cholinergic muscarinic receptors?

Metabotropic

3

What type of receptors are adrenergic receptors?

Metabotropic

4

Which autonomic system only utilises cholinergic receptors?

Parasympathetic system

5

What neurotransmitter is used at the NMJ?

Acetylcholine

6

What receptor type is found in the endplate at the NMJ?

Nicotinic

7

What four ways could NMJ transmission be inhibited?

1. Preventing acetylcholine being packaged into vesicle (E.g. Hemicholinium)
2. Blocking voltage gated Calcium ion channels so that calcium influx does not occur and so vesicle fusion with pre synaptic membrane will not occur.
(E.g. black widow spider toxin)
3. Preventing fusion of vesicles with pre synaptic membrane and so preventing acetylcholine release into the cleft.
(E.g. Botulinum toxin)
4. Use of competitive inhibitor to acetylcholine for the nicotinic receptors (E.g. D-tubocuranine)

8

What two ways could NMJ transmission be amplified?

1. Blocking voltage gated potassium ion channels. This way, entry of potassium ions cannot curtail the entry of calcium ions. More calcium ions can enter, stimulating the release of more neurotransmitter.
2. Blockage of acetylcholinesterase to prevent the breakdown of acetylcholine. It remains in the cleft to stimulate more nicotinic receptors.

9

How could pre-synaptic parasympathetic transmission be inhibited?

1. Preventing acetylcholine being packaged into vesicle (E.g. Hemicholinium)
2. Blocking voltage gated Calcium ion channels so that calcium influx does not occur and so vesicle fusion with pre synaptic membrane will not occur.
(E.g. black widow spider toxin)
3. Preventing fusion of vesicles with pre synaptic membrane and so preventing acetylcholine release into the cleft.
(E.g. Botulinum toxin)
4. Use of competitive inhibitor to acetylcholine for the nicotinic receptors (E.g. D-tubocuranine)

10

How could pre-synaptic parasympathetic transmission be amplified?

1. Blocking voltage gated potassium ion channels. This way, entry of potassium ions cannot curtail the entry of calcium ions. More calcium ions can enter, stimulating the release of more neurotransmitter.
2. Blockage of acetylcholinesterase to prevent the breakdown of acetylcholine. It remains in the cleft to stimulate more nicotinic receptors.

11

How could pre-synaptic sympathetic transmission be inhibited?

1. Preventing acetylcholine being packaged into vesicle (E.g. Hemicholinium)
2. Blocking voltage gated Calcium ion channels so that calcium influx does not occur and so vesicle fusion with pre synaptic membrane will not occur.
(E.g. black widow spider toxin)
3. Preventing fusion of vesicles with pre synaptic membrane and so preventing acetylcholine release into the cleft.
(E.g. Botulinum toxin)
4. Use of competitive inhibitor to acetylcholine for the nicotinic receptors (E.g. D-tubocuranine)

12

How could pre-synaptic sympathetic transmission be amplified?

1. Blocking voltage gated potassium ion channels. This way, entry of potassium ions cannot curtail the entry of calcium ions. More calcium ions can enter, stimulating the release of more neurotransmitter.
2. Blockage of acetylcholinesterase to prevent the breakdown of acetylcholine. It remains in the cleft to stimulate more nicotinic receptors.