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BMS 242 - Phys and pharm of cells > CNS pharmacology IV > Flashcards

CNS pharmacology IV Flashcards

1
Q

What are the 2 types of depression?

A

1) UNIPOLAR

2) BIPOLAR

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2
Q

What are the drugs used to treat depression?

A

Different depending on which type: unipolar or bipolar

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3
Q

What is unipolar depression?

A

Mood swings always in the same direction

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4
Q

What is unipolar depression characterised by?

A

Typical symptoms

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5
Q

What are the causes of unipolar depression?

A 
Reactive causes (75%)
- Specific triggers lead to the disease (eg. stressful situation)

Endogenous causes (25%)

  • No obvious cause
  • May be genetic components that underlie the disease
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6
Q

What is bipolar depression?

A

Low mood ALTERNATE with excessive positive feelings (mania)

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7
Q

What are the 3 causes of depression?

A
  • Stressful situation
  • Genetics
  • May be secondary to other illnesses (eg. Cushing’s disease)
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8
Q

What are the 4 brain regions implicated?

A

1) Nucleus accumbens and cingulate nucleus
2) Amigdala
3) Hippocampus

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9
Q

What is the amigdala part of in brain?

A

The LIMBIC SYSTEM

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10
Q

What is the amigdala involved in?

A

Fear responses in patients

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11
Q

What is the hippocampus involved in?

A

Important in controlling memory and learning

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12
Q

Where are the hormones Leptin and Ghrelin produced?

What are they involved in?

A

Produced in the periphery

Involved in feeding

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13
Q

What do the hormones Leptin and Ghrelin lead to changes in?

A

Stress signalling

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14
Q

How can postnatal depression effect the babies of the mother?

A
  • Depressed behaviour of the mother leads to epigenetic changes in the baby
  • Permanent susceptibility to depression through adult life
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15
Q

How can we study the brain changes in depression and the effects of anti-depressants be studied?

A

Cause prolonged stress to model animals and then treat them with anti-depressants and see how they react

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16
Q

How long does it take for anti-depressants to work in humans?

How can this be shown in animal models?

A

Takes several weeks

Seen in animal models that have been experiencing CHRONIC stressful situations (animal stressed in the unpredictable way each day)

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17
Q

What happens to mice that experience chronic stress?

A

Changes in the brain chemistry that is observed in the human conditions

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18
Q

How are the intermediate neuro chemical effects of antidepressants observed?

A

Observed in acute stressful situations (forced swim test, suspension test)

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19
Q

What is an obvious physical measure of depression?

A

High levels of blood CORTISOL

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20
Q

What is cortisol?

A

A stress hormone

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21
Q

What are the chemical causes of depression?

A

1) Depletion of the MONOAMINES in the brain

2) NDMA (glutamatergic) nerodegeneration

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22
Q

What are the 2 monoamine neurotransmitters that are involved in depression?

A

Serotonin (5-HT) and noradrenaline (NA)

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23
Q

As drugs that influence monoamine transmission (to treat depression) take several weeks to benefit, what does this show?

What did further research show?

A
  • Must involve long term trophic effects
  • Must somehow alter TRANSCRIPTION and RECEPTOR LEVELS in the effected neurons

Further research: revealed the possible role of BDNF and its receptor TrkB

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24
Q

What controls the levels of BDNF signalling?

A

Serotonin

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25
Q

What happens to the NA, 5-HT signalling in a depressed individual?

What does this lead to?

A

Reduced signalling through their receptors, leading to detrimental GENE TRANSCRIPTION

Leads to:

  • Loss of neurons through apoptosis
  • Loss of a number of active synapses
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26
Q

Normally, what do the 5-HT/NA receptors normally control?

A

Beneficial gene transcription

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27
Q

What happens to glutamate signalling in depression?

A

Excess activated of the NDMA receptors

Associated with neuronal loss

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28
Q

What is Ketamine?

What effects does it show in humans?

A

An anaesthetic

Shows effects in patients that are resistance to drugs in the NA-HT area

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29
Q

How does stress impact depression?

A

Through the effects on neurotransmission

30
Q

How does our understanding of the different neurotransmitter systems involved in depression?

A

Comes through the understanding of drugs that either CAUSE or ELEVATE depression

31
Q

What does iproniazid do?

What type of drug is this?

A

Elevates depression

An MAOI

32
Q

What does reserpine do?

How?

A

Causes depression

Through the depletion of the monoamine transmitter stores

33
Q

What do Tricyclic Acids?

A

Inhibit the re-uptake of 5-HT and/or NA

Effective in treating depression

34
Q

What are the 3 main classes of antidepressants?

A

1) MAOIs
2) TCAs (tricyclic antidepressants)
3) Selective serotonin re uptake inhibitors

35
Q

What is MAO involved in?

Where are they found?

A

The breakdown of amine neurotransmitters

Found on the inside and the outside of the neurons

36
Q

What are amine neurotransmitters?

A
  • Dopamine
  • Noradrenaline
  • Adrenaline
  • Histamine
  • Serotonin
37
Q

What are the 2 different type of MAOs?

Which one is the target of MAOIs? Why?

A

a and b subtypes

a subtype is the target of MAOIs as it is present in the CNS
b subunit is present in the PNS

38
Q

How do MAOIs work?

A
  • Inhibit MAO enzymes in the presynaptic terminal
  • Build up of amines in the cytosol
  • Amines leak out of the presynaptic terminal through the reversal of the transporters
39
Q

What are the side effects of the MAOI equivalent to?

A

The increase in sympathetic drive

40
Q

Why do some MAOIs have fewer side effects?

A

Target the a subtype more specifically (b subtype in the PNS)

41
Q

What level do TCAs work at the level of?

A

The level of the transporters of NA and 5-HT

42
Q

How do TCAs work?

A
  • Inhibit the transport of NaA and 5-HT by binding to the transporter
  • Neurotransmitters hang around in the synapse for longer
  • Increased activation of the receptors on both the presynapse/postsynapse
  • Increased activity through the receptors lead to their DESENSITISATION and DOWNREGULATION (takes a few weeks to be observed)
  • -> leads to alterations in excitability
  • Transcriptional changes
43
Q

What receptor is on the NA presynapse that is activated more strongly in the presence of TCAs?

What type of synapse is this?

A

Alpha-2-adrenoreceptors

Inhibitory synapse

44
Q

What do SSRIs show selectivity to?

A

Serotonergic signalling

45
Q

Are tricyclic antidepressants selective?

A

No

46
Q

Where do SSRIs work?

A

At the level of the transporters

47
Q

What does the effectiveness of the SSRIs depend upon?

A

The patient - all patients have different spectrums of the disorder

48
Q

What are TCAs and SSRIs drugs involved with?

A

5-HT

49
Q

What is the major source of NA?

What is it involved in?

A

The amygdala

Involved in regulating mood/arousal

50
Q

As well as mood and arousal, what is else is NA signalling involved with?

What does this mean?

A

Central regulation and blood pressure

  • Can lead to unwanted side effects with long-term use of antidepressants
  • Get low blood pressure
51
Q

Where is NA synthesised from?

A

Dopamine - from the amino acid tyrosine

52
Q

What is NA broken down by?

A

MAO and COMT

53
Q

What is the difference between the pathways of dopamine and NA?

A

NA neurons express dopamine beta-hydroxylase

54
Q

What is tyramine related to?

What disrupts tyramine processing?

A

Related to tyrosine

MAOI (antidepressants)

55
Q

What does the Raphe nucleus use as a neurotransmitter?

Where else in the body is this neurotransmitter used?

A

5-HT

Also used in regulating the limbic system

Also used as a neurotransmitter in the gut

56
Q

What are drugs that promote 5-HT transmission used to treat?

A

Depression
Anxiety
Migranes

57
Q

Why does the increase in 5-HT by medicines that treat depression have peripheral side effects?

A

5-HT is used as a neurotransmitter in the gut

58
Q

How is 5-HT synthesised?

A
  • From an amino acid TRYPTOPHAN

- Using TRYPTOPHAN HYDROXYLASE

59
Q

How is 5-HT broken down?

A

By MAO

60
Q

How do 5-HT and NA neurons interact with each other?

A

They are found in the SAME brain regions

They control the release of each other

61
Q

What are the selectivities of TCA and SSRI inhibitors?

A

VARY:

  • NA-selective
  • Non-selective
  • 5-HT selective
62
Q

What does CREB do?

How is CREB activated?

A

Controls the synthesis of BDNF

By the activation of serotonergic receptors in SOME parts of the brain that lead to the PHOSPHORYLATION of CREB

63
Q

What does BDNF do in NORMAL patients?

How?

A

Stabilised synaptic connects:

  • BDNF is released from the POSTSYNAPTIC site
  • Acts RETEROGRADELY on the nerve terminal forming the synapse
  • Action together –> strengthens the synapse
64
Q

What happens in relation to BDNF in DEPRESSED patients?

A
  • Reduced release of BDNF through the reduction in the synaptic activity
  • Synapses are not maintained –> less synapses/connections
65
Q

How do anti-depressant drugs strengthen signalling?

A

By increasing BDNF levels in the hippocampus

–> Leading to the re-establishment of the active synapses

66
Q

What accounts for the small, significant ultrastructural changes associated with depression?

A

Loss of synapses through the loss of BDNF

67
Q

What are alternative approaches to treating depression?

A
  • Anti epileptic drugs and anti psychotics –> mood stabilisers
  • ECT
68
Q

When are anti epileptic drugs and anti psychotics drugs used to treat depression?

A

In patients that show RESISTANCE to amine based approached

69
Q

Why is ECT effective?

A

Localised to SPECIFIC brain areas

Useful when patients are resistant to other types of drugs

70
Q

Why are the drugs used to treat bipolar disorders different to drugs in unipolar disorders?

A

Different neuro chemical bases

71
Q

What is used in the treatment of bipolar disorders?

How do they work?

A

Lithium

Inhibits IP3 receptors
Works on kinases

BMS 242 - Phys and pharm of cells (13 decks)

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