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NEUROPSYCH & CLINICAL NEURO > Week 4: Addiction neuroscience > Flashcards

Week 4: Addiction neuroscience Flashcards

1
Q

What is the definition of addiction?

A

There is no universally accepted definition

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2
Q

Addiction as a brain disease?

A

It has contributed to eliminating some of the stigmas associated with addiction

No longer considered moral failure or a lack of willpower

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3
Q

What is a criticism of addiction being seen as a brain disease?

A

It disregards human decision making and choice

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4
Q

What makes addiction different from classical diseases?

A

It is a group of behaviours, not an illness

Cannot be explained by a disease process

It is not an infectious disease

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5
Q

What does the DSM-5 call addiction?

A

It is under substance-related and addictive disorders

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6
Q

What are the 9 classes of drugs that may be involved in addiction?

A 
Alcohol 
Cannabis
Hallucinogens
PCP 
Opioids 
Inhalants 
Sedatives 
Stimulants 
Tobacco
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7
Q

The severity of an addiction depends on what?

A

How many criteria are met

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8
Q

What is a mild addiction?

A

2-3 criteria

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9
Q

What is a moderate addiction?

A

4-5 criteria

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10
Q

What is a severe addiction?

A

6+ criteria met

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11
Q

What is the cause of substance use disorders?

A

Thought to be a product of environmental and physiological factors

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12
Q

Explain positive reinforcement of drug addiction

A

Models suggest pleasurable effects of using a drug reinforce initial drug use

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13
Q

Over time, the rewarding effects of the drug are….

A

Reduced and drug-taking becomes compulsive

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14
Q

Explain negative reinforcement of drug addiction

A

When drug-taking behaviour is used as a way of achieving homeostasis (to feel normal or alleviate pain, discomfort or withdrawal)

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15
Q

Addiction shares features with which kind of disorders?

A

Impulsive and compulsive disorders

George Koob proposes that as an individual transit from an impulsive disorder to a compulsive disorder there is a shift from positive reinforcement to negative reinforcement driving the motivation for drug taking

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16
Q

Dopamine in parkinsons?

A

Those with Parkinsons have compromised levels of dopamine in their nucleus accumbens - they report blunted effects to stimulants

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17
Q

Opiates increase dopamine by…

A

Removing the inhibitory influence of GABA on dopamine-releasing cells

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18
Q

Addictive drugs activate reward pathways in the brain. How?

A

By triggering the release of dopamine

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19
Q

Drugs and LTP?

A

Cocaine exposure has been found to increase LTP in ventral tegmental areas lasting for days to months

Opioids, cannabis and alcohol all have been found to elicit LTP in mesolimbic and mesocortical projection areas

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20
Q

Dopamine in the nucleus accumbens?

A

It is a region in the central striatum that is heavily inadverted by dopamine fibres

  • Some drugs elevate dopamine transmission here
  • Food and sexual activity can also activate
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21
Q

Rats self-administering cocaine?

A

Dopamine levels in the nucleus accumbens increased during self-administration of intravenous cocaine

Dopamine antagonists decreased lever pressing by blocking the rewards of the drugs

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22
Q

What is gabapentin and what has it been found useful for?

A

It is a GABA agonist

Found to reduce drinking, decrease cravings in those with alcohol use disorder

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23
Q

Glutamate in addiction?

A

Addicts have lower levels of glutamate in their forebrains

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24
Q

What is synaptic plasticity?

A

The ability of synaptic connections to strengthen or weaken as a result of increased or decreased activity

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25
Q

Do those with substance use disorders have any differences in their white matter? What is an example of this?

A

Reduced white matter has been found in participants with substance use disorders.

A large number of studies have reported a significant loss of cerebral white matter found in postmortem and living individuals with alcohol use disorder

26
Q

What is LTP?

A

Long term potentiation

- Increased efficiency of neurotransmission with a critical role in learning and memory

27
Q

What happens to neurons with repeated drug use?

A

They adapt overtime - perhaps responsible for tolerance, addiction, and withdrawal

28
Q

What intracellular pathway in the brain is activated with the administration of addictive drugs?

A

Cyclic adenosine monophosphate (cAMP) pathway

29
Q

Are there any structural changes in the neurons of rats that self-administer cocaine? What might these changes lead to?

A

Prefrontal cortex
- Dendrites misshapen, large bulbous tips

Speculations claimed that these changes are linked to impaired decision making and judgements that are typical of human cocaine abusers

30
Q

What is grey matter?

A

Brain tissue containing cell bodies with unmyelinated axons

31
Q

Do drugs affect grey matter?

A

Studies have consistently reported gray matter volume reductions in the prefrontal regions and additional mesocorticolimbic structures

32
Q

What else might grey matter volume reductions be associated with?

A

Drug craving

33
Q

What is white matter?

A

refers to tracks of myelinated axons

34
Q

When exposed to substances in utero, are there any consequential differences in the brain?

A

Children exposed to cocaine, tobacco, marijuana, or alcohol in utero have smaller head circumference and white and gray matter relative to children not exposed to these substances

35
Q

Explain the changes in postsynaptic dopamine receptors in substance use disorders

A

Studies have found decreased density of D2 dopamine receptors in those with substance use disorders relative to controls

This is an important feature in addiction

36
Q

How do we measure dopamine release in the brain?

A

Binding assay combined with positron emission therapy

37
Q

What receptors are linked to the cAMP pathway?

A

Dopamine receptors

38
Q

What is raclopride used to measure and what is commonly seen with these measurements?

A

Used to measure dopamine levels through competitive binding to DA D2 receptors

If there is high raclopride binding - means low dopamine

If there is low raclopride binding - means high dopamine (more to compete and not as much binding)

39
Q

What happens to CREB when it is targetted by cAMP?

A

It becomes phosphorylated (becoming pCREB)

40
Q

What happens when there is an increased amount of phosphorylated CREB?

A

There is diminished sensitivity to drug-induced reward

41
Q

How is CREB linked with tolerance?

A

May provide a compensatory mechanism that responds to drugs

42
Q

Why can’t methylphenidate produce dopamine transmission in ex-cocaine abusers?

A

Suggests compromised activity of the dopamine system

As well as long-term neural adaption in that these are ex-users

43
Q

What does an over-expression of delta fosB lead to?

A

Increases sensitivity to the rewarding and reinforcement effects of stimulants

44
Q

Give an experimental example of drug escalation

A

When rats are exposed to a drug for self-administration over extended periods of time, they behave differently compared to rats with short access

With long access, the administration started to increase significantly from a certain point (drug escalation)

45
Q

How do we measure dopamine release in the brain?

A

Binding assay with combined with positron emission therapy

46
Q

What is the inability to experience pleasure called?

A

Anhedonia - very typical symptom in addiction

47
Q

What else might hypodopaminergia be associated with?

A

Hypofrontality - decreased activation in the prefrontal cortex

48
Q

What are the effects of methylphenidate similar to?

A

Similar to cocaine

49
Q

What happens when methylphenidate is used in controls and detoxified cocaine users?

A

Methylphenidate doesn’t have the same ability to produce increases in dopamine transmission of previous cocaine abusers

50
Q

Rat studies with alcohol and the over expression of D2 receptors?

A

As the amount of D2 receptors in the brain increased, the amount of alcohol intake decreased - consumed very little

High levels = decreased preference for the drug

51
Q

What are some interesting findings in IMPULSIVE rats?

A

They were found to have low dopamine D2 receptors
They also escalated to increased levels of self, they lose control - may be correlated with obtaining addiction -administration more than non-impulsive rats

52
Q

What is reduced dopamine transmission in the brain referred to as?

A

Hypodopaminergia

  • Depressive like symptoms
  • An inability or difficulty with experiencing pleasure
53
Q

How can hypodopaminergia be elicited in animals?

A

A drug called reserpine

54
Q

What is the inability to experience pleasure called?

A

Anhedonia - very typical symptom in addiciton

55
Q

What does hypofrontality impair?

A

Compromises planning and decision making - this is seen in those addicted to drugs

56
Q

How do dopamine D2 receptor levels influence the vulnerability of drug addiction?

A

High dopamine D2 receptors = more likely to report the effects of drugs such as methylphenidate as not pleasant

Low dopamine D2 receptors = more likely to report the effects of the drug as pleasant

57
Q

Rat studies with alcohol and the over expression of D2 receptors?

A

As the amount of D2 receptors in the brain increased, the amount of alcohol intake decreased

58
Q

What are some interesting findings in impulsive rats?

A

They were found to have low dopamine D2 receptors

They also escalated to increased levels of self-administration more than non-impulsive rats

59
Q

What else are low levels of dopamine D2 receptors associated with?

A 
Decreased activity (metabolism) in the orbitofrontal cortex 
- This is an area involved in controlling behaviour and impulse control (could be why we see deficits)
60
Q

Explain LTP and NMDA and AMPA receptors

A

NMDA receptors are occupied by glutamate
These NMDA channels open slightly to allow calcium into the cell
But these channels are blocked by magnesium

Magnesium can be removed by stimulation of AMPA receptors

  • these allow sodium into the cell, depolarises the membrane and dislodges the magnesium in the NMDA receptor
  • more AMPA are created, makes the cell more sensititve

NEUROPSYCH & CLINICAL NEURO (12 decks)

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