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Pharm > Lecture 14: Depression > Flashcards

Lecture 14: Depression Flashcards

1
Q

Which system in the brain controls emotions?

A

The Limbic System

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2
Q

Which system in the brain controls Motivation?

A

The Mesocorticolimbic dopamine system

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3
Q

What three elements of behavior does depression distrupt?

A
  • Cognition
  • Emotion
  • Motivation
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4
Q

What does the motivation system do?

A

Drives behavior that is purposeful and goal directed

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5
Q

What is the Limbic brain?

A

A cortical border circling the brainstem

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6
Q

What parts does the limbic brain include?

A
  • Hippocampus
  • Amygdala
  • Basal Ganglia
  • Cingulate Gyrus
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7
Q

What is one of the oldest parts of the cortex?

A

The limbic brain

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8
Q

How does depression affect the limbic region and striatum?

A

Major depression causes increased engagement of the limbic regions and decreased engagement of regions involved in motivation (striatum) compared to healthy controls

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9
Q

What is activity in the brain driven by?

A

Neurotransmitter release or changes in the postsynaptic response

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10
Q

What are the monoaminergic neurotransmitters?

A
  • Dopamine
  • Norepinephrine
  • Serotonin
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11
Q

What neurotransmitters is the limbic system heavily concentrated with?

A

Monoamine neurotransmitters

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12
Q

What is the difference between the monoaminergic neurotransmitters and Glutamate and GABA?

A

The monoamine neurotransmitters are more modulatory as opposed to glutamate and GABA which are more excitatory and inhibitory

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13
Q

What precursor do Adrenaline and Dopamine both start with?

A

Tyrosine

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14
Q

What does tyrosine hydroxylase (TH) do?

A

Converterts Tyrosine to L-dopa

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15
Q

What does L-Dopa get converted into?

A

Dopamine

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16
Q

What does Dopamine B-hydroxylase do?

A

Converts dopamine into noradrenaline

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17
Q

What is the precursor to Serotonin?

A

Tryptophan

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18
Q

What does L-amino acid decarboxylase (AADC) do?

A

Converts L-Dopa to Dopamine and 5-HTP to Serotonin

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19
Q

What does Tryptophan hydroxylase do?

A

Converts Tryptophan to 5-HTP

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20
Q

What enzyme degrades all three of the monoamine neurotransmitters?

A

Monoamine Oxidase (MAO)

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21
Q

What kind of behavior is Dopamine important for?

A

Motivate behavior

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22
Q

What do most of the drugs to treat depression target?

A

Norepinephrine and the serotonergic system

23
Q

What does the Amine Hypothesis of Depression state?

A

That depression results from inadequate monoamine neurotransmission (serotonin and noradrenaline)

24
Q

What was Reserpine initially used as?

A

A hypertensive drug used to HBP

25
Q

How is Reserpine related to depression?

A

It was found that people who took reserpine developed a syndrome indistinguishable from depression

26
Q

How does Reserpine cause its depressive effect?

A

It depletes neurons of dopamine and norepinephrine

27
Q

What happens to Dopamine after it is synthesized?

A

It is packaged into vesicles and can either be released as dopamine or it can be converted to norepinephrine by dopamine b-hydroxylase

28
Q

What is required of dopamine before it can be released in the synapse and bind to receptors?

A

It must be packaged into vesicles

29
Q

What does Reserpine block?

A

The transporter that is necessary for moving dopamine into vesicles

30
Q

How is Iproniazid related to depression?

A

Patients who took Iproniazid tended to have their symptoms alleviated

31
Q

What enzyme does Iproniazid inhibit?

A

Monoamine Oxidase (MAO), the enzyme responsible for the breakdown of monoamines

32
Q

What are the problems with the amine hypothesis of depression?

A
  • Drugs that restore monoaminergic levels are only moderately effective in 30-50% of patients
  • Inconclusive evidence that serotonin and noradrenergic systems are disrupted in depression
  • Antidepressants to several weeks before clinical effect is seen, despite immediate effects on synaptic neurotransmitter levels
33
Q

What does the Glutamate hypothesis of depression state?

A

Depression is associated with reduction in glutamatergic signalling in the cortex

34
Q

What does the loss of Glutamatergic signalling impact?

A

Excitatory and inhibitory function leading to a reduced signal to noise. It also impacts LTP, neurotrophic production (BDNF), synapse formation and gene transcription

35
Q

What receptors do inhibitory GABAergic neurons have?

A

NMDA glutamate receptors

36
Q

What are the most common antidepressants?

A

MAO inhibitors

37
Q

What do MAO inhibitors do?

A

They increase synaptic levels of monoamine neurotransmitters (norepinephrine and serotonin)

38
Q

What is an example of an MAO drug?

A

Iproniazid

39
Q

What diet must be followed with MAO inhibitors?

A

A low tyramine diet

40
Q

What is the tyramine cheese reaction?

A

When eating a meal rich in tyramine while taking a MAO inhibitor can lead to acute hypertension cause by tyramine binding to adrenergic blood vessels and in the heart

41
Q

What is Tyramine?

A

A sympathomimetic monoamine (acts like noradrenaline) and is naturally found in certain foods

42
Q

What is Tyramine degraded by?

A

MAO

43
Q

What does Tyramine bind to?

A

Alpha and Beta adrenergic receptors in the heart and activates them

44
Q

What do the selective reuptake inhibitors block?

A

The serotonin (SET) or noradrenaline transporters (NET)

45
Q

What do the serotonin (SET) or noradrenaline transporters (NET) do?

A

Move the neurotransmitters from the synapse to the intracellular space

46
Q

What happens when serotonin (SET) or noradrenaline transporters (NET) are blocked by Selective Reuptake inhibitors?

A

They inhibit both NET and SET from removing neurotransmitters from the synapse

46
Q

What happens when serotonin (SET) or noradrenaline transporters (NET) are blocked by SSRIs or SNRIs?

A

The increase levels of serotonin or norepinephrine at the synapse

47
Q

What are the side effects of MAOIs, SSRIs, and SSRIs?

A
  • Nausea
  • Indigestion
  • Dizziness
  • Dry mouth
  • Weight loss
48
Q

Where is 90% of serotonin found?

A

In the GI tract

49
Q

What does Ketamine do at the receptor?

A

It is a noncompetitive NMDA receptor antagonist

50
Q

What receptor does Ketamine bind to and where does it bind on the receptor?

A

It binds to glutamate receptors but binds to them inside the pore

51
Q

What does Ketamine binding to NMDA receptors on GABA interneurons do?

A

It blocks its ability to open and pass positively charged ions

52
Q

How does Ketamine work?

A

It blocks NMDA glutamate receptors on GABA neurons causing a burst in glutamate causing synaptic remodelling and resetting of glutamate and GABA systems because it blocks the inhibition by GABA of glutamate neurons

53
Q

What is the therapeutic index of Ketamine?

A

It has a very narrow therapeutic index

Pharm (31 decks)

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