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PSYC 361 > Module 4 > Flashcards

Module 4 Flashcards

1
Q

What are 3 classes of drugs?

A
  • Depressants: alcohol, opiods, tranquilizers (e.g., barbiturates, benzodiazepines, and sleep aides)
  • Stimulants (excitants): amphetamines, cocoaine, caffeine and nicotine
  • Hallucinogens: psychedelics, dissociatives (e.g., PCP, ketamine, N2O), and deliriants (indigenous plants, Benadryl, and nutmeg)
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2
Q

What are some problems with labelling drugs into the 3 categories of depressant, stimulant, and hallucinogen? (4)

A
  • Labels are influence by experienced drug effects: sometimes induced NS function changes and drug use experiences match well, sometimes not that simple
  • Hallucinogens’ effects can be generated by both CNS stimulant and depressant properties
  • Alcohol is typically labelled as a depressant, but it may have stimulant properties
  • Nicotine also has both stimulant and depressant properties
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3
Q

What are 3 medical uses of drugs?

A
  • Anesthesia/analgesia: e.g., ketamine, opiods
  • Treatment for pain: opiods, cannabis
  • Treatment for mental disorders: e.g., benzodiazepines for anxiety and insomnia
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4
Q

What are the general principles of drug action?

A

PSychoactive drugs alter the nervous system functions by altering neurotransmission.
Synaptic signalling can be increased or decreased, and can be modulated pre- or post-synaptically.

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5
Q

How does cocaine/amphetamine work?

A

Block DA reuptake transporter. In addition, amphetamine stimulates tyrosine hydroxylase (DA synthesis) and inhibit MAO (degradation).

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6
Q

How do opiods work?

A

Activates receptors that inhibit GABAergic interneurons in the mesolimbic and nigrostriatal DAergic pathways to increase DA levels in NAcc

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7
Q

How does alcohol work?

A

No known receptors for alcohol, but it can potentiate GABA recpetors.
Acute, low-dose alcohol use is shown to increase striatal DA activity. Large dose acts as CNS depressant. May also interact w/ neuropeptide systems.

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8
Q

How does nicotine work?

A

Activate nicotinic acetylcholine receptors (nAChRs). Nicotine use activates nAchRs in the VTA to increase DA levels in the NAcc.

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9
Q

What 4 basic categories does the diagnostic criteria for substance use disorder have?

A
  • impaired control
  • physical dependence
  • social problems
  • risky use
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10
Q

What motivational changes occur during addiction? (4)

A
  • Pathologicallly elevated motivation for drug seeking and drug use (wanting)
  • Drug-related cues trigger stronger drug-related responses
  • Drug dependence can develop, which results from the NS’s maladaptive functional changes in response to repeated drug use
  • Tolerance may also develop, and sometimes reverse tolerance, such that the same amount of drug produces a smaller hedonic experience (liking)
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11
Q

What are 4 commonly used behavioural paradigms to study addiction in animals?

A
  • Conditioned place preference
  • Self-administration (in operant chamber)
  • Locomotor sensitization
  • Some other anxiety-based paradigms
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12
Q

What is conditioned place preference?

A

Based on classical conditioning principles. Animals associate the distinct context in which drugs are administered, and later develop a preference for that context when given a choice.

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13
Q

What is the conditioned compensatory response, and how can it contribute to the development of addiction? (4)

A
  • Over repeated drug use, the body learns about the drug’s effects and will produce physiological responses to counteract these changes
  • Can dampen the drug’s psychological and physiological effects (tolerance)
  • Can produce the opposite effects w/o drug in the system (withdrawal symptoms)
  • Failure to elicit the conditioned compensatory response in the absence of drug cues or in a novel context can result in a lack of compensation, leading to overdose
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14
Q

What is the self-administration paradigm of addiction?

A

Based on operant conditioning principles. Intravenous self-administration (IVSA) works similarly to ICSS, in which drug delivery produces a reinforcing effect and sustains the behaviour through +ve reinforcement.

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15
Q

What is found when extended drug access is given to rodents? (2)

A

Leads to addictive-like behaviour:
- Long cocaine IVSA (6+ hours) increases frequency and total amt of self-administered cocaine over days

Makes drug seeking compulsive
- Reduced the ability of shock-paired cues to suppress drug-seeking, even though fear to CS is still present!

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16
Q

Which stages of the addiction cycle does extended drug access coincide with?

A
  • Increasing drug use
  • loss of control over drug-use
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17
Q

What does the extinction-reinstatement paradigm study?

A

Used to study withdrawal, abstinence, and relapse stages of the addiction cycle

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18
Q

Describe the stages of the extinction-reinstatement paradigm

A
  1. Self-administration
  2. Extinction
  3. Reinstatement:
    - cue-induced OR
    - drug-induced OR
    - stress-induced
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19
Q

What is the relationship between the oFC and addiction? (3)

A
  • Reduced function of oFC in cocaine abusers (hypofrontality)
  • Hypofrontality correlated w/ decreased D2 receptor binding in the ventral striatum/NAcc
  • Compromised oFC function decreases top-down control in drug use
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20
Q

How is the vmPFC implicated in addiction?

A

Substance abusers who perform poorly on IGT also fail to show a GSR in anticipation of making a risky decision

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21
Q

What is the relationship between amphetamine use and decision-making quality?

A

Duration of drug use predicts decision making quality.
- Longer duration of drug use predicts lower quality of decision-making

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22
Q

What kind of drug access shows the highest number of responses per 1mg of cocaine?

A

Intermittent access

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23
Q

What is relationship between abstinence of drug use and amount of response in prescence of drug-associated environmental cues?

A

The prescence of cues elicits reinstatement after a longer period of withdrawal

24
Q

What is the lifetime prevalence for substance use disorder?

A

~15%

25
Q

How prevalent is the development of SUD in those who experiment with addictive drugs?

A

~17.5-22%

26
Q

What components does a good theory of addiction have? (4)

A
  • Pleasure
  • Tolerance
  • Withdrawal symptoms
  • Relapse
    Successful theories address these components, and ideally for all addictive substances
27
Q

How is dopamine involved in locomotor sensitization? (4)

A
  • Repeated to addictive drugs increases locomotor response, can induce a hyperdopaminergic state
  • Associated with increased evoked and basal levels of DA in the NAcc
  • Sensitization appears to be mediated by alterations in neural circuits linking the PFC, NAcc and VTA
  • Sensitized rats show increased responding for conditioned reinforcers locomotion DA levels
28
Q

How does a hyperdopaminergic state alter incentive in conditioned reinforcement?

A

In a hyperdopaminergic state, cues (conditioned reinforcer) exert an increase level of response

29
Q

What pathways and brain regions are implicated in the dopamine-related theories of addiciton? (4)

A
  • VTA
  • Limbic system
  • PFC control
  • DA recpetors in the NAcc
30
Q

What do learning theories of addiction argue? (3)

A
  • Addiction stems from disorders of normal learning processes
  • Drug seeking and use behaviour is product of pathological learning
  • Addiction can be understood by understanding learning and memory mechanisms
31
Q

What two types of contingencies underly addiction in the context of learning theories?

A
  • Cues and drugs: what cues indicate drug
  • Actions and drugs: what you do to get drug
32
Q

What is the mechanism of drug addiction according to learning theories? (4)

A
  • Drug use is initiated as goal-directed behaviour
  • Repeated drug use leads to habit formation (learning), then drug cues and environment gain control over behaviour, even when the hedonic effects have reduced
  • May also impair retrieval/utilization of knowledge (inhibiting drug use), thus, impair the control by specific outcomes/contingencies
  • Chronic drug use leads to a ventral-to-dorsal (goal-to-habit) striatal switch in behavioural control
33
Q

What supports the learning theories of addiction? (3)

A
  • Drug cues can elicit craving, drug-related behaviour, and relapse
  • Devaluation procedure demonstrated goal-direct and habit-controlled behaviour in humans and animal models taking addictive drugs
  • Ventral-dorsal transition observed as increased DA release from NAcc core (ventral) during early stage, and in the dorsal striatum during late stage of addiction
34
Q

What is a challenge with learning theories of addiction?

A

Habit-controlled responding often does not occur under complex decision scenarios, suggesting the goal-directed component is still present, but may be distorted

35
Q

How does incentive sensitization theory describe drug addiction?

A

Repeated exposure to addictive drugs changes the brain circuitry that regulates incentive salience attribution. Cues associated with drug eventually take over behaviour of the person using drugs.

36
Q

Describe the development of addiction using incentive sensitization theory (5)

A
  • Initial drug use for pleasurable effects
  • Tolerance develops over time, however effect of drug-associated cues becomes sensitized
  • Stimuli that are imbued with incentive salience can elicit approach behaviour, energize ongoing actions, and act as reinforcers
  • Multiple cues can activate the neural networks that trigger unconscious conditioned responses that collectively may be viewed as craving
  • Cues lead to more drug intake, even if the effects are not as pleasurable anymore
37
Q

How does incentive sensitization theory work mechanistically (neural underpinnings)? (3)

A
  • Addictive drugs increase mesocorticolimbic DA neurotransmission
  • Mesocorticolimbic DA system functions to attribute incentive salience to contexts, cues and oher events that are associated with activation of this DAergic system (drug taking)
  • Repeated exposure to addictive drugs produces enduring neuroadaptations to sensitize the DA system’s response to drugs and drug-associated cues
38
Q

What support does the incentive sensitization theory of addiction have? (2)

A
  • Prior drug experience enhances the rewarding effects of drugs later (self-reported)
  • In animal models and humans, repeated amphetamine administration leads to more DA responses, and performance in various behavioural paradigms is influenced by sensitization
39
Q

What is the challenge with incentive sensitization theory?

A

Does not account for withdrawal, and to some extent, tolerance

40
Q

Describe D1R and D2R

A

D1R: low affinity, need higher DA concentrations to activate, likely requires burst firing/phasic activity. Burst firing may be elicited by cues, gaining control over behaviour
D2R: high affinity, need lower DA concentrations to activate, tonic activity is sufficient

41
Q

Which suggested 6 neural circuits does the DA imbalance model of addiction affect?

A
  1. Reward/salience
  2. Motivation
  3. Learning + Memory (including associations and habit)
  4. Inhib control and executive function
  5. Interoception
  6. Aversion avoidance and stress reactivity

Adiction is theorized to be the result of disruption of the balance between these circuits

42
Q

What support is there for the DA Imbalance Theory of addiction? (3)

A
  • Striatal DA activity is stimulated byaddictive drugs, and correlates with self-reported euphoria
  • Striatal-PFC inhibitory control through D2R is also implicated
  • Acknowledges the stress reactivity in addiction
43
Q

What is the frontostriatal dysfunction theory of addiciton? (3)

A
  • Based on “hypofrontality”, the theory proposes that repeated exposure to addictive drugs compromises top-down executive control over behaviour
  • Drug-induced brain changes lead to impaired cortical inhib (mPFC and OFC) and mesolimbic activity (amygdala and NAcc), that together produce compulsive drug-related behaviour
  • A DA imbalance model sub-theory, only describes relapse
44
Q

How does the opponent process theory explain emotional responses? (5)

A
  • The A- and B-processes develop consequently and temporally (but independently)
  • A-process overlaps w/ the onset and termination of the stimulus
  • B-process develops later and remains activated after stimulus termination
  • Once B-process decays, the body/emotion returns to homeostatic baseline
  • Repeated exposure to the stimulus leads to earlier/stronger development of the B-process
45
Q

Describe the hedonic-allostasis theory of addiction (4)

A

An expansion of the opponent process theory:
- Chronic drug use leads to decreases in the hedonic effects and increases in activation of the anti-reward/stress-related systems
- Dysregulation of the reward and anti-reward systms leads to a permanent deviation from the previous setpoint of reward, fueling drug-related behaviour and vulnerability to relapse
- Points to limitastions of “homeostatic view”, rather, these motivational changes appear to allostatic, more enduring and is achieved by rebalancing the homeostatic changes
- Hypothesized that changes in the cortico-striatal-thalaic circuits are involved in addiction, may be in the form of either within- or between-system neuroadaptations

46
Q

What are DNA methyl transferases (DNMTs)?

A

Enzymes that add methyl groups to DNA molecules, inhibiting gene expresion

47
Q

What are the consequences of histone acetylation?

A

Increased gene expression, by opening space between histones

48
Q

How does maternal RNA function in epigenetic regulation?

A

Maternal RNAs function as transcription factors that initiate early stages of development

49
Q

How do experiences induce epigenetic responses? (5)

A
  • Epigenetic changes are extremely sensitive to environmental information
  • Epigenetic changes accumulate
  • Epigenetic modifications are inheritable
  • Gene expression patterns within cells determine the fate and the physiological functions of them
  • Epigenome is analogous to a huge database that stores info about experience
50
Q

For how many generations does transgenerational memory of pathogen avoidance last and is this memory transmitted?

A

4 generations. At the 5th generation, the organism displays the original behaviour
- TGF-β gene is regulated by the piRNAs in a specific pair of sensory neurons to mediate this memory

51
Q

What is the relationship between ΔFosB expression in the hippocampus and conditioned placed preference in the context of cocaine use?

A

Cocaine use induced ΔFosB expression, and is correlated with stronger CPP
- Disruption of chromatin remodelling represses ΔFosB expression and suppresses CPP

52
Q

What are 3 pieces of evidence for the transgenerational effects of drug use?

A
  • Maternal cannabis exposure enhances morphine induced CPP in F1 progeny
  • Paternal alcohol exposure leads to F1 preference for alcohol
  • Paternal nicotine exposure leads to more locomotor activity in F1
53
Q

What evidence is there for ELS affecting the HPA axis through epigenetic regulation? (3)

A
  • Maternal care alters GR density in the hippocampus
  • Maternal separation exaggerates the expression deficiency and leads to behavioural alterations in baby rhesus monkeys
  • Serotonin transporter regulates stress hormone receptor (GR+MR) expression levels in the PFC and hippocampus in an ELS-dependent fashion
54
Q

What is the first identified epigenetic marker of ELS, and how was it studied by Nieratschker et al. (2014)?

A

MORC1:
- Found similar methylation patterns in humans, rhesus monkeys and rats from ELS
- Statistically significantly correlated with MDD (altho had replication issues with the results later possibly due to MDD heterogeneity)

55
Q

How can ELS increase an individual’s risk for addiction through epigenetic regulation? (3)

A
  • ELS is strong predictor of stress-related disorders later in life, with alterations in the HPA axis, and 5-HT and BDNF pathways
  • Individuals with ELS may have abnormal stress responses and compromised neural resources for coping
  • ELS increases individuals’ susceptibility to addiction when drug is provided in the face of stressful events
56
Q

What are some roles that epigenetics play in addiction? (3)

A
  • Drug exposure leaves epigenetic signatures
  • ELS-induced epigenetic changes may increase the risk of addiction in affected individuals
  • Epigenetic changes often accompany behavioural changes in experimental paradigms

PSYC 361 (4 decks)

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