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Flashcards in Drug action in CNS Deck (27)
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1

Describe the structure of a neurone

Composed of cell body, dendrites, axon and axon terminal
Dendrites receive information from other neurones
Cell body contains nucleus, stores DNA and rough ER which builds protein and mitochondria
Axon carries information in form of electrical signal i.e. action potential
Axon terminal converts chemical signal into electrical signal and releases neurotransmitters

2

In which region do neurones communicate with one another?

Synapse

3

Synaptic transmission can only be chemical. True or false?

False can be electrical or chemical
Electrical synapses are very rare in the adult brain

4

What is the gap at the chemical synapse between the pre and post synaptic neurones called?

Synaptic cleft

5

What happens when an AP reaches the pre-synaptic terminal?

Ca2+ channels open and neurotransmitter release is initiated

6

Where in the synapse are neurotransmitters stored?

Pre-synaptic terminal

7

How is ACh synthesised?

Acetyl CoA + choline --> ACh + coenzyme A
Choline acetyltransferase is an enzyme which transfers an acetate ion from acetyl coA to choline. It is specific to cholinergic neurones and present in neuronal terminal in excess i.e. not saturated

8

What is the effect of increasing the amount of choline in terms of ACh synthesis?

You can increase the synthesis of ACh

9

Where is ACh stored?

Synaptic vesicles in the axonal terminal

10

When is ACh released?

Released into the synaptic cleft upon arrival of an AP and influx of Ca2+

11

When ACh is released, where does it bind?

Binds to post-synaptic receptors - muscarinic (M1 and M5) and nicotinic

12

What are the 5 subunits that nicotinic receptors are composed of?

Alpha, beta, gamma, epsilon and delta

13

Nicotinic receptors are divided into two main types. What are they?

Muscle and neuronal

14

Where are muscle nicotinic receptors located?

Neuromuscular junction

15

Where are neuronal nicotinic receptors located?

Autonomic ganglia and CNS

16

What is ACh broken down by?

Acetyl cholinesterase breaks it down into acetate ion and choline molecule. Choline is transported back to pre-synaptic terminal

17

What is the role of autoreceptors and where are they located?

Located on pre-synaptic terminal. They are activated by neurotransmitter and can control the synthesis or release of a neurotransmitter - almost like a feedback loop

18

What is the neuromuscular junction?

A chemical synapse between a motor neurone and skeletal muscle fibre

19

How does the action of ACh at the NMJ cause muscle to contract?

AP -> motor neurone -> Ca2+ release and ACh release.
ACh binds to nicotinic receptors on post-synaptic neurone and they open -> Na+ release -> depolarisation. AP then generated in skeletal muscle -> Ca2+ release -> contraction

20

Name a disorder that affects the NMJ

Myasthenia Gravis

21

What is myasthenia gravis?

An autoimmune condition that prevents muscles from contracting as a result of damage to the muscle acetylcholine receptors

22

Which drug is used in myasthenia gravis to improve symptoms and how does it work?

Pyridostigmine - cholinesterase inhibitor so prevents the breakdown of ACh and improves muscle contraction

23

How is dopamine synthesised?

L-tyrosine -> L-dopa -> Dopamine

24

Which post-synaptic receptors does dopamine bind to upon being released?

D1 family - excitatory
D2 family - inhibitory

25

What are the two ways in which dopamine can be inactivated?

Metabolic enzymes - COMT and MOA
Reuptake processes - catecholamines and DAT

26

What are ionotropic receptors?

Receptor is part of ligand-gated ion channel protein and activation results in ion conductance changes. Receptor is opened by transmitter to allow passage of either Na+ (excitatory) or K+/Cl- (inhibitory). They are involved in fast transmission

27

Describe metabotropic receptors

The receptor protein in the membrane is coupled to effector mechanism via G-proteins. In this signalling mechanism, agonist molecule combines with receptor proteins in the membrane. The resulting conformational change causes activation of membrane-associated enzymes via G-protein