Modulation of Neurotransmission

Question 1

Are synapses excitatory or inhibitory?

Answer 1

Can be either, depending on the NT type and the nature of the post-synaptic receptors.

Question 2

What are the steps of synaptic transmission?

Answer 2

1. NT synthesis in synaptic terminal or neuronal cell body (peptides)
2. NT released due to AP and Ca entry
3. NT interacts with receptor across cleft
4. Enzymatic degredation in cleft or in presynaptic terminal post-reultake

Question 3

What enzymes are commonly used for enzymatic degradation?

Answer 3

MAO: monoamine oxidase
AChE: acetylcholinesterase

Question 4

How is a SA node AP different to a ventricular AP?

Answer 4

No fast Na channels
No plateau phase as we don’t need contraction
NaIf current present so slow depolatisation

Question 5

How do vagal and sympathetic transmitters interact presynaptically?

Answer 5

ACh inhibits the cardiac sympathetic terminal and NPY inhibits the cardiac vagal terminal.

Question 6

What NTs have been involved in depression development?

Answer 6

Serotonin
Dopamine
NA

Question 7

Pontine NA system: origin

Answer 7

Locus coeruleus in pons

Question 8

Serotonin system: origin

Answer 8

Brainstem raphe nuclei

Question 9

Midbrain dopamine system: origin

Answer 9

Substantia nigra and VTA

Question 10

What is the monoamine theory of depression?

Answer 10

If antidepressant drugs help sx by increasing NT levels then surely the symptoms were caused by low NT levels in the first place?

Question 11

What are the inconsistencies with this theory?

Answer 11

With drugs monoamines increase fast but 2-3 weeks for effect
Some drugs eg. cocaine increase monoamine NT but don’t fix it
Clinically ineffective in many patients

Question 12

Where is dopamine released from/to to cause pleasurable sensation?

Answer 12

From the nucleus accumbens, made in the VTA. These neurons are activated by 5HT (which then autoinhibits raphe neurons from which it’s released)

Question 13

Auto-inhibition of 5HT neurons

Answer 13

1. Normally 5HT1A autoreceptors limit spontaneous activity of the serotoninergic neuron
2. In depression these are hypersensitive so inhibit activity completely
3. SSRI treatment increases serotonin and desensitises the receptors, restoring normal activity.

Question 14

Neuroinflammation theory of depression

Answer 14

New! Sickness behaviour correlates with depression so maybe brain release of inflammatory cytokines causes an action on the brain?

Question 15

What are microglia?

Answer 15

Reuptake NTs esp. glutamate
Important for synaptic plasticity
Control BBB and chemical environment
Release cytokines

Question 16

What happens to microglia in chronic stress?

Answer 16

Increase

Question 17

What do antidepressants to do microglia activity?

Answer 17

Decrease activation and decrease their release of cytokines without involving serotonin (some other antidepressants also do this).

Question 18

How long is a sleep cycle and what proportion SWS and REM is it?

Answer 18

90 mins
80% SWS
20% REM

Question 19

What stage of sleep does growth hormone peak at?

Answer 19

Stage 4 SWS

Question 20

What brain structures modulate sleep?

Answer 20

Suprachiasmatic nucleus of the hypothalamus is the brain’s biological clock (has clock genes, responds to light)

• Sends messages to forebrain (attention and emotions), pineal gland (melatonin), hypothalamus (hormonal control, orexin and temperature modulation)
• Brainstem does sleep/arousal state

Question 21

What are orexins?

Answer 21

Neuropeptides made in the dorsal hypothalamus that control appetite and arousal