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Biopsych > Neurotransmitter system dysfunction > Flashcards

Neurotransmitter system dysfunction Flashcards

1
Q

What is the process for an action potential- neurotransmitter release to occur?

A

1- Action potential
2- Vesicle Docks
3- Neurotransmitter release (exocytosis)
4- NT binds to receptor
5- Unbound NT transported into pre synaptic terminal
6- NT gets broken down or repackaged into vesicles

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2
Q

What are the 5 main types of monoamines

A 
Adrenalin
Noradrenaline
Dopamine
Serotonin
Melatonin
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3
Q

What are the 3 catecholamines?

A

Adrenalin
Noradrenaline
Dopamine

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4
Q

What are the 2 Indolamines?

A

Serotonin

Melatonin

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5
Q

What are the 2 symptoms of Monoamine System Dysfunction as a result of psychostimulant drug abuse

A

Paranoid psychosis- similar to schizophrenia
Depression
Anxiety
Parkinson’s like symptoms

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6
Q

What are the schizophrenia symptoms

A

1- Psychotic ‘positive’ symptoms (episodic)- delusions, hallucinations, thought disorders
2- Deficit ‘negative’ symptoms (chronic)- disturbances in :motivation, experience of pleasure, social interactions, spontaneous speech, mood expression- prevent them from having social behaviour
3- Cognitive impairment (chronic)- intellectual, memory, executive function, attention
*

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7
Q

what are the symptoms for the positive symptoms

A

Hallucinations- usually auditory (single or multiple)
Delusions (paranoid)- persecution, grandiosity, external thought control, thoughts inserted or removed, mind read
Thought disorder- tangential, loosening associations, garbage

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8
Q

What are the 4 NT’s involved in schizophrenia

A

Dopamine
Serotonin
Glutamate
GABA

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9
Q

what is the dopamine hypothesis of schizophrenia

A

drugs that increase dopamine levels in the nucleus accumbens exacerbate or produce positive psychotic symptoms (cocaine, amphetamine, dopamine receptor agonists)

Drugs which block dopamine transmission alleviate some of the symptoms of schizophrenia (dopamine antagonists)

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10
Q

where do schizophrenics have an increase and decrease of dopamine?

A

Schizophrenics have increased dopamine in the nucleus accumbens and decreased dopamine in the prefrontal cortex

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11
Q

what happens when there is too much dopamine in the nucleus accumbens?

A

Increased dopamine= positive symptoms (psychoses). euphoria at beginning

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12
Q

What happens when there is less dopamine in the prefrontal cortex?

A

Hypofrontality: Cognitive deficits, negative symptoms

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13
Q

How are the positive psychotic symptoms produced?

A

By increased dopamine in the nucleus accumbens (mesolimbic dopamine)

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14
Q

How are the negative and cognitive symptoms produced?

A

by decreased dopamine in the prefrontal coretex (mesocortical)

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15
Q

How does dopamine influence the filter in the dorsal striatum?

A

It weakens the filter, meaning it increases the salience of the information, which you then pay attention to everything and cannot filter out what is good and what is unimportant information

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16
Q

How do you stop the amount of dopamine from going through the filter?

A

Use a dopamine D2 receptor antagonist to prevent psychoses

17
Q

What are the two first generation typical antipsychotics? ‘neuroleptics’

A

Chlorpromazine, haloperidol

18
Q

What do antipsychotics do?

A

They bind and block dopamine D2 receptors and make them more effective at reducing psychotic symptoms
If they have better bidning to D2 receptors, they have more clinical potency

19
Q

What was the problem with the first generation neuroleptics (antipsychotics)

A

They antagonised both D1 and D2 receptors,
no effect on negative and cognitive symptoms
Ineffective in %30 of patients
Exacerbate symptoms in some
20% relapse rate
5-10% have intolerable side effects (due to many receptors involved)

20
Q

What do typical neuroleptics block?

A

D1 and D2 receptors

21
Q

What do D2 receptors do?

A

produce positive psychotic symptoms

22
Q

What do D1 receptors do?

A

Maintain normal movement

23
Q

what system is crucial for movement?

A

Substantia Nigra dopamine system.

Decreased dopamine in nigrostriatal causes Parkinson’s. Blocks D1 and D2 receptors interrupts our ability to move.

24
Q

What is the pyramidal system?

A

Pre motor cortex
Supplementary Motor Area
goes to
Spinal cord and muscles for voluntary movement

25
Q

What is the extrapyramidal system?

A

Nigrostriatal dopamine and substantia niagra- goes to Caudate/Basal ganglia which helps rythmic/phasic movement- subconscious e.g. walking

26
Q

How do extrapyramidal side effects occur?

A

For it to be a successful anti-psychotic, 80% of the receptors need to be blocked. Of these, 80% of these also affect D1 receptors by the consumption of drugs

27
Q

What are extrapyramidal side effects?

A

Parkinson’s like symptoms e.g. acute dystonias (involuntary movements), muscle spasms and protruding tongue.
Tardive Dyskinesia- debilitating movement disorder.

28
Q

What are the next typical antipsychotics?

A

Sulpride

29
Q

What is the pros and cons of Sulpride?

A

Highly selective for D2 receptors
Less extrapyramidal side effects
Still not effect on negative or cognitive symptom- need to address prefrontal cortex deficits

30
Q

What is the suicide rate for depression if left untreated?

A

15%

31
Q

What is the monoamine hypothesis?

A

The effectiveness of a monoamine oxidase inhibitor to elevate mood in depressed patients indicated that the depletion of monoamines contributed to the pathology of depression

32
Q

What are the main brain regions involved in depression?

A

Hippocampus, prefrontal cortex, amgydala, nucleus accumbens

33
Q

what are the 2 first generation anti-depressants?

A

Tricyclic Antidepressants- block re-uptake of all monoamines

Monoamine Oxidase inhibitors- block the metabolism of active monoamines

34
Q

What are the receptors that the monoamine neurons could be working with?

A

Noradrenaline—Alpha or beta receptors
Dopamine—-D1 or D5 receptors
Serotonin—- 5-HT1A receptors

35
Q

What are the steps with Monoamine neurotransmission

A

1- Action potential- release of monoamine (nora, dopa, sero)
2-Monoamines bind to receptors
3- Coupling or binding to G protein, and second messenger systems may or may not be activated
4- Activated systems produce an excititory post synaptic potential, and the inhibitory protein causes an inhibitory post synaptic potential
5- Monoamines leave binding sites and get taken up via the respective transporters

36
Q

What G protein doesnt activate a second messenger?

A

GI

37
Q

What are the transporters for the monoamines?

A

Nora- NET
Dopa- DAT
Sero- SERT

38
Q

what do TCA’s (tripsychic anti depressants) do?

A

Block the re-uptake of all monoamines

Biopsych (14 decks)

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