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PSGY1005 Addiction and the Brain > introduction to addiction and the brain > Flashcards

introduction to addiction and the brain Flashcards

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The Brain flashcards
1
Q

define neuropharmacology

A

branch of pharmacology that deals with the action of drugs on the nervous system

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2
Q

what is a neurotransmitter?

A

naturally occurring chemical that carry chemical signals (messages) from one neuron (nerve cell) to the next target cell

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3
Q

define psychotropic

A

drugs that affect a person’s mental state

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4
Q

identify 4 classic neurotransmitters involved in addiction

A
  • dopamine
  • noradrenaline
  • serotonin
  • acetylcholine
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5
Q

what is another name for serotonin?

A

5-hydroxytryptamine, 5-HT

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6
Q

what drugs release neurotransmitter dopamine?

A

amphetamines
cocaine

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7
Q

what drugs release neurotransmitter noradrenaline?

A

amphetamines
cocaine

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8
Q

what drugs increase serotonin?

A

ecstasy (MDMA)

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9
Q

what drug activates acetylcholine receptors?

A

nicotine

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10
Q

what is chemical transmission?

A

the way a signal gets from one neuron/brain cell to the next

chemical transmission relies on number of different signalling pathways and chemical systems

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11
Q

why do we have neurotransmitters?

A

due to the need for communication within the brain and the rest of nervous system

neuron and nerve cells need to communicate with eac hother

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12
Q

describe the nerve transmission process

A

dendrites -> cell body (soma) -> axon -> axon terminal

  • neural signals travel electrically along nerve fibres
  • neurotransmitters cross a synaptic gap/cleft between nerve cells to reach next neuron
  • crosses synaptic cleft through process of diffusion
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13
Q

what are neurotransmitters stored in?

A

synaptic vesicles

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14
Q

how are neurotransmitters received at end of axon terminal?

A
  • receptors
  • these are specially configured to receive and be activated by the neurotransmitter that is released
  • this unlocks a postsynaptic response as an ‘agonist’
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15
Q

what is similar about psychotropic drugs and neurotransmitters and how does this affect receptors?

A
  • psychotropic drugs and neurotransmitters have similar chemical structures
  • meaning they can activate or block receptors that are intended to recognise brain’s own neurotransmitters
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16
Q

what is it meant by ‘AGONIST’ with regards to neurotransmitters?

A
  • AGONISTS are substances that bind to synaptic receptors
  • these INCREASE the effect of neurotransmitter
  • has the net effect to increase neurotransmission (as a direct or indirect agonist)
17
Q

what is it meant by ‘ANTAGONIST’ with regards to neurotransmitters?

A
  • ANTAGONISTS are substances that bind to synaptic receptors
  • these DECREASE the effect of a neurotransmitter (these block receptor)
  • has the net effect to decrease neurotransmission (as a direct or indirect antagonist)
18
Q

what do ‘autoreceptors’ do?

A
  • found presynaptically
  • act like thermostats
  • regulate neurotransmitter release and neuronal firing at neuron terminal and cell body
  • neurotransmitters/drugs acting here can reduce further release at the termal so further neurotransmission is reduced
19
Q

what effect can drugs have on synaptic transmission?

A
  • can have a net positive effect (as direct or indirect agonist)
  • can have a net negative effect (as direct or indirect antagonist)
20
Q

give an example of drug action that acts as an agonist

A

amphetamines

stimulate release of dopamine and noradrenaline

21
Q

give an example of drug action that acts as an antagonist

A

cocaine

blocks the reuptake of dopamine and noradrenaline

22
Q

What are the short term effects of MDMA/Ecstasy?

Gerra et al. (2000) study looking at the effects of MDMA/ecstasy

A
  • drug increases serotonergic (5-HT)
  • serotonergic = affecting serotonin neurotransmitter
  • drug increases levels of serotonin
23
Q

What is the suggested long term effect of MDMA/Ecstasy?

Gerra et al. (2000) study looking at the effects of MDMA/ecstasy

A
  • evidence that serotonin can become depleted
  • indicating neurotoxicity (altering of normal activity of nervous system)
  • results in cell death in serotonergic pathways
24
Q

Outline Gerra et al. (2000) study looking at the effects of MDMA/ecstasy

A
  • uses an indirect measure to look at effect
  • looks at measuring serotonergic function indirectly
  • done by issuing challenge test
  • fenfluramine is a drug that increases serotonin release
  • increased serotonin has effect on pituitary gland –> this is shown as hormonal change (specifically prolactin response
  • plasma prolactin is looked at to measure the effect of fenfluramine
  • a normal response should show that an increase of fenfluramine would results in an increase in plasma prolactin as fenfluramine increases serotonin which increases hormonal response of prolactin
25
Q

Outline findings of Gerra et al. (2000) study looking at the effects of MDMA/ecstasy

A

‘normal’ volunteers
- show an increased prolactin response to fenfluramine
- consistent with what was expected of normal response

‘MDMA’ users
- showed a reduced prolactin response to fenfluramine
- suggests that MDMA users serotonergic function is depressed
- additionally, reduced response to prolactin persists in ppts who previously used MDMA but do not presently

  • suggests long term effects of long term use of MDMA
  • evidence consistent with neurotoxicity and death of pathways –> if change was functional, some recovery would be expected when drug use stops but this is not the case
25
Q

Outline findings of Gerra et al. (2000) study looking at the effects of MDMA/ecstasy

A

‘normal’ volunteers
- show an increased prolactin response to fenfluramine
- consistent with what was expected of normal response

‘MDMA’ users
- showed a reduced prolactin response to fenfluramine
- suggests that MDMA users serotonergic function is depressed
- additionally, reduced response to prolactin persists in ppts who previously used MDMA but do not presently

  • suggests long term effects of long term use of MDMA
  • evidence consistent with neurotoxicity and death of pathways –> if change was functional, some recovery would be expected when drug use stops but this is not the case
26
Q

Outline Miczek & Mutschler (1996) study looking at the effects of social stress in lab animals

A
  • lab animals used
  • social stress brings about physiological response
  • rats trained to respond by pressing level for cocaine or food reward
  • before social stress introduced, rats responded more for lever
  • social stress introduced
  • social stress manufactured by placing an ‘intruder’ which was another male rat
  • intruder would attack (wire mesh placed to prevent injury)
  • lasted 60 minutes
  • after social stress, rats showed increase response for cocaine but not for food reward
  • shows selective effect of social stress on cocaine-reinforced responding
  • shows drug as very powerful reward
27
Q

How does Miczek & Mutschler (1996) rat study apply to addiction in humans?

A
  • suggests role of stressful life events in relapse of human drug users

PSGY1005 Addiction and the Brain (18 decks)

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