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

CNS pharmacology IV Flashcards

(71 cards)

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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
What happens to the NA, 5-HT signalling in a depressed individual? What does this lead to?
Reduced signalling through their receptors, leading to detrimental GENE TRANSCRIPTION Leads to: - Loss of neurons through apoptosis - Loss of a number of active synapses
26
Normally, what do the 5-HT/NA receptors normally control?
Beneficial gene transcription
27
What happens to glutamate signalling in depression?
Excess activated of the NDMA receptors Associated with neuronal loss
28
What is Ketamine? What effects does it show in humans?
An anaesthetic Shows effects in patients that are resistance to drugs in the NA-HT area
29
How does stress impact depression?
Through the effects on neurotransmission
30
How does our understanding of the different neurotransmitter systems involved in depression?
Comes through the understanding of drugs that either CAUSE or ELEVATE depression
31
What does iproniazid do? What type of drug is this?
Elevates depression An MAOI
32
What does reserpine do? How?
Causes depression Through the depletion of the monoamine transmitter stores
33
What do Tricyclic Acids?
Inhibit the re-uptake of 5-HT and/or NA Effective in treating depression
34
What are the 3 main classes of antidepressants?
1) MAOIs 2) TCAs (tricyclic antidepressants) 3) Selective serotonin re uptake inhibitors
35
What is MAO involved in? Where are they found?
The breakdown of amine neurotransmitters Found on the inside and the outside of the neurons
36
What are amine neurotransmitters?
- Dopamine - Noradrenaline - Adrenaline - Histamine - Serotonin
37
What are the 2 different type of MAOs? Which one is the target of MAOIs? Why?
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
How do MAOIs work?
- 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
What are the side effects of the MAOI equivalent to?
The increase in sympathetic drive
40
Why do some MAOIs have fewer side effects?
Target the a subtype more specifically (b subtype in the PNS)
41
What level do TCAs work at the level of?
The level of the transporters of NA and 5-HT
42
How do TCAs work?
- 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
What receptor is on the NA presynapse that is activated more strongly in the presence of TCAs? What type of synapse is this?
Alpha-2-adrenoreceptors Inhibitory synapse
44
What do SSRIs show selectivity to?
Serotonergic signalling
45
Are tricyclic antidepressants selective?
No
46
Where do SSRIs work?
At the level of the transporters
47
What does the effectiveness of the SSRIs depend upon?
The patient - all patients have different spectrums of the disorder
48
What are TCAs and SSRIs drugs involved with?
5-HT
49
What is the major source of NA? What is it involved in?
The amygdala Involved in regulating mood/arousal
50
As well as mood and arousal, what is else is NA signalling involved with? What does this mean?
Central regulation and blood pressure - Can lead to unwanted side effects with long-term use of antidepressants - Get low blood pressure
51
Where is NA synthesised from?
Dopamine - from the amino acid tyrosine
52
What is NA broken down by?
MAO and COMT
53
What is the difference between the pathways of dopamine and NA?
NA neurons express dopamine beta-hydroxylase
54
What is tyramine related to? What disrupts tyramine processing?
Related to tyrosine MAOI (antidepressants)
55
What does the Raphe nucleus use as a neurotransmitter? Where else in the body is this neurotransmitter used?
5-HT Also used in regulating the limbic system Also used as a neurotransmitter in the gut
56
What are drugs that promote 5-HT transmission used to treat?
Depression Anxiety Migranes
57
Why does the increase in 5-HT by medicines that treat depression have peripheral side effects?
5-HT is used as a neurotransmitter in the gut
58
How is 5-HT synthesised?
- From an amino acid TRYPTOPHAN | - Using TRYPTOPHAN HYDROXYLASE
59
How is 5-HT broken down?
By MAO
60
How do 5-HT and NA neurons interact with each other?
They are found in the SAME brain regions They control the release of each other
61
What are the selectivities of TCA and SSRI inhibitors?
VARY: - NA-selective - Non-selective - 5-HT selective
62
What does CREB do? How is CREB activated?
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
What does BDNF do in NORMAL patients? How?
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
What happens in relation to BDNF in DEPRESSED patients?
- Reduced release of BDNF through the reduction in the synaptic activity - Synapses are not maintained --> less synapses/connections
65
How do anti-depressant drugs strengthen signalling?
By increasing BDNF levels in the hippocampus --> Leading to the re-establishment of the active synapses
66
What accounts for the small, significant ultrastructural changes associated with depression?
Loss of synapses through the loss of BDNF
67
What are alternative approaches to treating depression?
- Anti epileptic drugs and anti psychotics --> mood stabilisers - ECT
68
When are anti epileptic drugs and anti psychotics drugs used to treat depression?
In patients that show RESISTANCE to amine based approached
69
Why is ECT effective?
Localised to SPECIFIC brain areas Useful when patients are resistant to other types of drugs
70
Why are the drugs used to treat bipolar disorders different to drugs in unipolar disorders?
Different neuro chemical bases
71
What is used in the treatment of bipolar disorders? How do they work?
Lithium Inhibits IP3 receptors Works on kinases

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

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