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PSY325 > Week 4 - Addiction > Flashcards

Week 4 - Addiction Flashcards

1
Q

What is anhedonia?

A

Inability of experiencing pleasure

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2
Q

What is hypodopaminergia?

A

Depletion of monoamine stores in the brain that can cause depressive-like symptoms

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3
Q

Hypodopaminergia is linked to ________ and ____________.

A

Anhedonia

Hypofrontality

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4
Q

What is hypofrontality?

A

Decrease in activation of prefrontal cortex, which compromises planning and decision-making

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5
Q

According to Volkow ND et al (2007), what did the brain scans of alcoholics show?

A

DA decreased and reported reduced reinforcing effects of MP

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6
Q

According to Volcow et al (1997), what id the brain scans of cocaine abusers show?

A

Decreased DA and reported reduced rewarding effects of MP

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7
Q

What is a challenging problem in the neurobiology of drug addiction?

A

To understand why some individuals become addicted to drugs while others do not.

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8
Q

What may be one of the keys to determining why some people become addicted to drugs while others do not?

A

Differences in reward circuits: dopamine levels and receptor levels

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9
Q

What happens when there is an over-expression of D2 receptors in the NAcb in rats addicted to alcohol?

A

Reduces alcohol preference and alcohol self-administration

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10
Q

What does a form on impulsivity in rats predict?

A

high rates of intravenous cocaine self-administration

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11
Q

A form of impulsivity in rats predicts high rates of intravenous cocaine self-administration. What is this associated with?

A

Changes in dopamine (DA) function before drug exposure

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12
Q

What did Dally et al find while using PET on rats and cocaine reinforcement?

A

D2/3 receptor availability is significantly reduced in the nucleus accumbens of impulsive rates that were never exposed to cocaine

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13
Q

In humans, what were low densities of dopamine D2 receptors associated with?

A

Decreased metabolism in the orbitofrontal cortex, where metabolism in other regions (basal ganglia) was relatively normal.

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14
Q

What psychological disorder is associated with decreased metabolic activity in the orbitofrontal cortex?

A

Obsessive-compulsive disorder (OCD)

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15
Q

What neurotransmitter does Ritalin (ADHD drug) bind to?

A

Dopamine (DA) receptors

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16
Q

Long-term addiction results in ____

A

Long-term adaptations to the dopamine system

reduced activity of dopamine

reduced experience of pleasure

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17
Q

Low levels of D2 receptors are associated with……

A

Increased desire for drugs

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18
Q

What are some criticisms for the brain-based view of addiction?

A

It disregards human decision making and choice

Addiction is not a disease in the classical sense:

  • It’s a group of behaviours, not an illness in its own right
  • It can’t be explained by the disease process
  • There is no infectious disease or common biological degenerative or neuropathological problem
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19
Q

What is tolerance?

A

The need for increased amounts of the substance to achieve the desired effect

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20
Q

What is addiction a product of?

A

Environmental and physiological factors

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21
Q

How does the addiction cycle begin?

A

Positive reinforcement

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22
Q

How does the addiction cycle change over time?

A

Switches from positive reinforcement to negative reinforcement

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23
Q

What disorders contribute to addiction?

A

Impulsive and compulsive disorders

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24
Q

What did George Koob suggest about addiction?

A

An individual transits from an impulse disorder to a compulsive disorder, there is a shift from positive reinforcement to negative reinforcement

25
Q

What complex connections between brain regions are referred to in relation to reward pathways?

A

Striatal, midbrain, limbic and prefrontal regions known as the mesocorticolimbic pathways

26
Q

What pathway is made up of the striatal, midbrain, limbic and prefrontal regions?

A

Mesocorticolimbic

27
Q

Why do we need to talk about “reward systems’ with caution?

A
  • Some say the brain have evolved to express dedicated neural systems specifically for encoding reward or pleasure
  • It is more likely that it has dedicated systems for motivating behaviour (which is positively reinforced) to survive (eg. feeding etc) and drugs interact and compromise these systems
28
Q

Which brain area has elevated dopamine transmission when drugs such as amphetamine, cocaine, nicotine and morphine are taken?

A

Nucleus accumbens (a region of the ventral striatum heavily innervated by dopamine fibres)

29
Q

What brain region has increased dopamine transmission when eating and having sex?

A

Nucleus accumbens

30
Q

What receptors are critically involved in long-term potentiation?

A

NMDA and AMPA

31
Q

What did Wise et al (1995) discover about dopamine levels in the nucleus accumbens in rats?

A

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

32
Q

How did dopamine antagonists affect lever-pressing behaviour in rats?

A

Decreased lever-pressing behaviour and lesioning of the nucleus accumbens drastically reduce the rate of drug administration

33
Q

What is Pargyline?

A

MAO inhibitor and prolongs the actions of 6-OHDA

34
Q

How do dopamine antagonists affect the rewarding effects of drugs?

A

block the rewarding effects of drugs

35
Q

How is dopamine related to Parkinsons disease?

A

People with Parkinson’s disease are known to have compromised levels of dopamine in the nucleus accumbens and mesollimbic pathways

36
Q

What did patients of parkinson’s disease indicate about drugs of abuse?

A

They report blunted effects of stimulants, which supports the role of dopamine in the rewarding effects of drugs of abuse

37
Q

What is Anhedonia?

A

Failure to experience rewarding stimuli

38
Q

Lazenberge (2010) argued that, in addition to the dopamine system, the __________ _______ plays a critical role in mediating the experience of _________ evidenced by a voluminous body of ________-________ research.

A
  1. Serotonergic system
  2. pleasure
  3. depression-related
39
Q

What did Self (2004) report about opiates and GABA?

A

Reported that opiates increase dopamine in part by removing the inhibitory influence of GABA neurons on dopamine-releasing cells

40
Q

What is gabapentin?

A

A GABA agonist that has been found to reduce drinking, cravings, improve sleep and affect in participants with alcohol use disorder

41
Q

What changes are associated with addiction?

A

a) synaptic plasticity
b) dendritic size and spines
c) changes in white and gray matter
d) up/down - regulation of receptors
e) changes in intracellular signalling pathways

42
Q

What is long-term potentiation?

A

Efficiency of neurotransmission and plays a critical role in learning and memory

43
Q

How does cocaine exposure effect long-term potentiation?

A

Has been found to increase LTP in the ventral tegmental area, lasting for days to months after cessation of treatment

44
Q

How do opioids, cannabis and alcohol effect long-term potentiation?

A

Been found to elicit LTP in mesolimbic and mesocortical projection areas such as the nucleus accumbens, hippocampus, amygdala and prefrontal cortex

45
Q

What happens to rats during exposure to psychostimulants?

A

Leads to sensitised locomotor responding to these drugs when rats are re-exposed to the drug weeks-to-months later

46
Q

Repeated exposure to psychostimulants facilitates the acquisition of drug ______-________.

A

Self-administration

47
Q

What is enhanced by sensitisation in animals?

A

Subsequent reinstatement of drug-seeking as well as the amount of work animals will produce to self-administer the drug

48
Q

How does sensitisation affect dopamine neurons?

A

Enhances the excitability of dopamine neurons

49
Q

How do amphetamines change dendrites?

A

Increased size of dendritic arbours

Increased number of spines

Elevates number of glutamatergic synapses

50
Q

Where did Robinson et al (2001) find structural changes in neurons in rats that self-administered cocaine?

A

Neurons in the prefrontal cortex

51
Q

What is gray matter?

A

Brain tissue containing cell bodies with unmyelinated axons

52
Q

What has research found about gray matter volume and density in substance use disorders including alcohol, nicotine, meth and cocaine?

A

Reductions in gray matter volume in prefrontal regions and additional mesocorticolimbic structures

53
Q

What have studies shown about gray matter and drug craving?

A

Drug craving was negatively associated with gray-matter in the insula, prefrontal cortex, amygdala, temporal cortex, occipital cortex, cerebellum and thalamus

54
Q

What is white matter?

A

Tracks of myelinated axons

55
Q

What did Rivkin et al (2008) report about children who were exposed to cocaine, tobacco, marijuana or alcohol in utero?

A

They had smaller head circumference and white and grey matter relative to children not exposed to these substances

56
Q

What is CREB?

A

One of the most studied molecules targetted by cAMP

its a protein that plays a key role in learning and memory

57
Q

What is correlated with an increase in phosphorylated CREB?

A

Diminished sensitivity to drug-induced reward

58
Q

What did Eric Nestler postulate about CREB and drugs?

A

CREB provides a compensatory mechanism that responds to drugs and that could be linked wth tolerance and with symptoms of dysphoria and withdrawal, but could also play a more general role in signalling the response to stimuli with strong emotional salience

59
Q

What activates CREB?

A

Morphine treatements in the nucleus accumbens

Stressors such as foot-shock and social stress

PSY325 (11 decks)

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