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Biopsychology and Learning > Substance abuse > Flashcards

Substance abuse Flashcards

1
Q

What are 5 kinds of drugs of abuse?

A

Many substances are abused by humans
Major Stimulants
Narcotics
Cannabis
Nicotine
Alcohol

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2
Q

What do stimulants do?

A

Stimulant : arouses or accelerates activities

Psychostimulant : stimulates the brain
Not just physical stim, stim the brain as well

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3
Q

What do narcotics do?

A

induces narcosis (sleep or stupor) = numbing

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4
Q

What do hallucinogens do?

A

produce hallucinations

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5
Q

How has meth usage changed with time?

A

Methamphetamine use is stable BUT more potent forms used from 2013
In 2013, ppl started taking crystal meth instead (more pure)
The amount of ppl taking meth stayed the same, but the type they take changed (became more potent)
Most ppl who take meth are under some sort of psych distress
Methamphetamine use is stable BUT it is used at high frequently
Not just higher purity but also used more frequently Increases the health burden on our society and economic burden bc addicts dont participate in society as much

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6
Q

Why do we take drugs?

A

Simple: they make us feel good

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7
Q

What is the reward pathway?

A

Mesolimbic Dopamine
Nucleus accumbens(NA): Major Reward Area
Ventral Tegmental Area: VTA, Dopamine cell bodies
Reward is governed by DA
VTA projects to accumbens = mesolimbic syst

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8
Q

What is reward?

A
  • Reward: positive reinforcement, smtg thatll make you do smtg again
  • Initial exposure to certain drugs will produce feelings of reward:
    – Elation
    – Excitement
    – Relaxation
    Depending on the drug you take Usage
    Reinforced (repeated) - becomes a drug of abuse
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9
Q

What makes a substance rewarding?

A

All drugs of abuse aug DA in Accumbens
* Ability to increase dopamine in the nucleus accumbens
* Natural rewards (sex, food, nurturing) also increase dopamine in the nucleus accumbens (Very involved in motivational processes and survival)

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10
Q

How do rats self stimulate and self administer?

A
  • Rats will self stimulate (electrically)
  • Median Forebrain Bundle (monoamine fibres of passage)
  • Nucleus Accumbens
  • Lateral Hypothalamus
    VTA going to accumbens, causes release of DA in accumbens if stim these axons
    Rats will self stim bc its rewarding
    Rats will also self-administer drugs intravenously
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11
Q

What 5 facts are evidence that DA = reward?

A
  1. Rats will self-stimulate the medial forebrain bundle which is inhibited by dopamine receptor antagonists (blockers)
    Dont self stim if dont get effect of DA
  2. Natural rewards (food, sex) increase dopamine neurotransmission
  3. Rats will self-administer dopamine-like drugs and most drugs of abuse
  4. Drugs of abuse increase dopamine neurotransmission
  5. The rewarding effect of abused drugs is inhibited by dopamine receptor antagonists and lesions of dopamine cells (6-OHDA)
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12
Q

What is the Activity of dopaminergic neurons in a lever press task like?

A
  • Initially reward presentation causes a burst of firing but this dies off as the task is learned
    DA cells are really interested in the saliency of things, when learn, fire less, still involved but not as much
  • Wrong choices which result in no reward causes a silencing of the neuron at the point when reward was expected
    Signals a reward prediction error
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13
Q

What is the link between DA and predicted reward?

A
  • The anticipation of reward produces a large increase in dopamine
  • The reward itself produces some dopamine release, yet an error in the value of the reward has more of an effect on dopamine
  • “better than expected” enhances dopamine signalling
    If an unexpected, better reward is presented dopamine levels would greatly increase
    The pharmacology of drugs to enhance dopamine levels signals to the brain that the drug is much “better than expected”
    The drug becomes really salient
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14
Q

What are 5 short term effects of stimulants?

A
  • Euphoria & well-being
  • Increased alertness
  • Increased self-confidence
  • Increased energy
    Ecstasy (MDMA) is also an ENTACTOGEN (touchy feely)- promotes closeness to others
    causes release of oxytocin
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15
Q

What do psychostimulants do?

A

increase extracellular monoamines

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16
Q

What is the pharmacology of coke?

A

Modulation of DAT increases dopamine in synaptic cleft

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17
Q

What is the pharmacology of ampphetamines?

A

Amphetamines increase extracellular monoamines
Reverse monoamine and vesicular transporters (VMAT)
Methamphetamine reverses the DAT & VMAT, inhibits monoamine oxidase (MAO)
“Ecstasy” (a type of amphetamine) reverses the SERT (SERotonin Transporter)
Can deplete DA levels very fast so if dont have good diet, wont build it back up

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18
Q

What do coke and amphetamine do?

A

Amphetamine affects similar regions to cocaine
Both increase dopamine transmission by activity at DAT
Striatum -stereotypy (repetitive movement)

19
Q

What are 5 side effects of stimulant use?

A
  • Seizures
  • Depression & Anxiety
  • Paranoia
  • Psychosis
  • Neurotoxicity
20
Q

What is the pharmacology of weed?

A

Active constituent of Cannabis is D9-Tetrahydrocannabinol (THC)
THC binds to Cannabinoid receptors to increase DA release in the nucleus accumbens
CBD doesnt have psychoactive properties but its and anxiolytic, anticonvulsant, can help to stop take meth
Cannabinoid receptors: CB1 & CB2
Anandamide is the natural ligand for these receptors (Endocannabinoid)

21
Q

What are the effects of weed?

A

Cortex: motor/sensory
Cingulate cortex: judgement
Hippocampus: blunts memory
Cerebellum: blunts motor coordination

22
Q

What is the pharmacology of nicotine and alcohol?

A

Both increase dopamine release in nucleus accumbens by modulation of different receptor types:
* Nicotine - Nicotinic receptors (Acetylcholine)

  • Alcohol: Works on lots of diff receptors, depends on the alcohol you drink
  • GABA-A receptor agonist; inhi cell firing (sedative)
  • NMDA glutamate receptor antagonist
  • Modulates opioid peptide system (mu receptors)
23
Q

What is Amphetamine-induced Neurotoxicity?

A

Excess use of MDMA
Reduced Serotonin Transporters
Transporters deplete bc the terminals die off
Ecstasy reverses the Serotonin Transporter (SERT) and causes serotonin depletion in neurons
Loss of serotonin, serotonin metabolites and transporters.
Cell bodies are still intact but function abnormally
Just the terminal died off, the brain though it wasnt needed bc there was no more 5HT
In monkeys who have been treated with ecstasy regeneration of serotonin cells is very slow

24
Q

Repeated use of ecstasy can lead to what? (5)

A

Depleted stores of serotonin in the terminals
Neurotoxicity(death) of serotonin cell terminals
Chronic depressive and/or anxiety states
Reductions in social interaction
Increases in Anxiety

25
Q

Prolonged use of meth can lead to what?

A

Methamphetamine may also produce depletions in serotonin to produce depressive and anxiety symptoms
More likely to cause a depletion of DA
Methamphetamine has a greater effect on dopamine neurons
* Neurotoxicity of dopamine neurons (Nigrostriatal)
* Reduced dopamine increases the filter of the basal ganglia information for movement can not get through
* Cases of Parkinson’s Disease (PD)-like symptoms have been reported
* Similar to the ‘frozen addicts’ who took MPTP by mistake

26
Q

Chronic use of Methcathinone can lead to what?

A

Decreases DAT binding
Chronic drug use has long-term behavioural consequences due to sustained modulation of neurotransmitter systems

27
Q

What is Substance Use Disorder?

A

Its when you start doing things that are maladaptive, inappropriate bvr bc the only thing that you seek is drugs, when nothing other than drugs matter
A state characterized by: A compulsion to take drugs continuously or periodically
* Experience rewarding effects (A)
* Avoid the discomfort of its absence (B)
Allostasis = just trying to feel normal, your homeostatic gets worse and worse, take drugs to try and feel normal

28
Q

Physical vs psychological dependance?

A

Physical dependence
* Stop taking the drug produces withdrawal symptoms
* Heroin - abrupt cessation causes sweating, goose-pimples, diarrhoea, muscular spasms, aches and pains
* Alcohol and benzodiazepines (valium) - hypersensitivity to sound and light, anxiety, convulsions, coma and even occasionally death (if withdrawal is too abrupt)

Psychological dependence
* Craving of the drug during abstinence

29
Q

What are 4 components of substance use disorder?

A
  • Tolerance - loss of effect of a drug (reward) with repeated administration get less of a high the more you take the drug, the R get used to that amunt of drug
  • Withdrawal - appearance of symptoms associated with termination of chronic drug use, brain’s used to getting it and looks for it when its no longer there
  • Neuroadaptive processes to counter the acute effects of the drug
    A key element in drug dependence is also sensitisation:
  • the increased ‘response’ to a drug following repeated administration
    Not reward, the anxiety and psychotic responses, negative sides get worse bc of neuroplasticity
  • LONG TERM (chronic) neuroadaptations which are manifest after repeated drug administration
30
Q

Liking vs wanting

A
  • Incentive-sensitization theory of addiction
  • Compulsive drug use & inability to stop (relapse)
  • ‘Excessive amplification’ of wanting the drug
  • Less reliance on ‘liking’ the drug
    Less of A and want the drug to avoid B

4 Main components
* Addictive drugs share the ability to cause enduring neural adaptations
* Neural adaptations occur in regions involved in incentive motivation and reward (mesolimbic/mesocortical)
* These regions become hypersensitive (sensitized)
* But instead of sensitizing the reward (liking) component, drug ‘wanting’ is now dominant (need the drug). The brain has changed to accommodate maladaptive behaviour

31
Q

What makes a substance addictive?

A
  • Speed and magnitude of increased dopamine in the nucleus accumbens
  • “RUSH”
    Determined by:
  • Potency
  • Route of administration
    – Oral
    – Subcutaneous
    – Intramuscular
    – Intranasal (snorting)
    – Inhalation
    – Intravenous
32
Q

What are the 4 limitations of the dopamine theory of addiction?

A
  1. Aversive stimuli such as the stress of handling, electric footshock, tailpinch or aggressive attacks increase dopamine transmission
  2. Mice lacking the dopamine transporter (DAT) will still self-administer cocaine (remember cocaine blocks the DAT)
  3. Individual differences - all abused drugs increase dopamine transmission but only a small percentage of people become addicted
  4. A major component of addiction is craving. Animal models of drug addiction (behavioural sensitisation and drug selfadministration) show that the major neurotransmitter involved in craving is glutamate (learned associations with environmental cues - prefrontal & orbitofrontal cortex).
    Learned association with drug taking will send glut in accumbens and cause craving
33
Q

What are 3 symptoms arising from drug addiction?

A
  • Anxiety
  • Depression
  • Psychosis
    May be treated with available pharmacotherapies
    Pharmacotherapies for addiction arent good
34
Q

What are animal models of addiction?

A

Ø Common animal model of drug addiction is the drug ‘self-administration’ technique
Ø Animals (mice, rats, monkeys) will lever press to receive intravenous infusions of most drugs abused by humans (esp. cocaine, amphetamine, heroin, nicotine, but not LSD, THC?)
Ø Rats will self-administer alcohol orally
Ø Rats will also ‘self-stimulate’ brain areas associated with reward
Rats will self-administer cocaine until death (90%)
Heroin less toxic at 36% deaths
Rewarding effect of cocaine is blocked by dopamine receptor antagonists

35
Q

What are the once off effects of coke and amphetamine?

A

Amphetamine affects similar regions to cocaine
Both increase dopamine transmission by activity at DAT
Striatum - stereotypy (repetitive movement)

36
Q

What are the effects of repeated use of coke and amphetamine?

A

Nucleus Accumbens: Motivation, Reward & Reinforcement
Hippocampus & Amygdala: Memory & Emotion
Dorsal Striatum: Decisions & Habit formation
Prefrontal Cortex: Decisions & Control (appropriate behaviour)
Orbitofrontal Cortex: Drive (value of reward)

37
Q

What does drug use do to striatal activity?

A

Drug use increases activity in Striatum: activity correlates with perceived “rush”
Aug DA = aug Saliency of drug
Inflates reward prediction error
You think that taking the drug is more imp than it is bc of the pharmacology of the drug
Addicts: DA response to natural rewards is reduced or absent, they’re only interested in the drug

38
Q

What does drug use do to orbitofrontal cortex activity?

A

Shift in Saliency by Increased Activation of Orbitofrontal Cortex
When you show a non addict a pic of smtg rewarding, they have activity in the OFC but addicts dont bc the drug hijacked their brain and shifted the saliency of rewards
OFC activity increased while drug-taking only in addicts
The OFC enhances the reinforcing properties of the drug- compulsive drug seeking & usage

39
Q

What do the hippocampus and amygdala do after drug use?

A

Hippocampus & Amygdala remind Addict of how good drug use feels
Cravings
Lots more activity in dorsolateral PFC, parahippocampal gyrus and amygdala than non craver

40
Q

What do associations with drug use do in the accumbens?

A

Associations With Drug-taking Stimulates Glutamate Transmission to Nucleus Accumbens
Anterior cingulate cortex, DL PFC, OFC and Amygdala neurons contain glutamate which signals to neurons in the nucleus accumbens
Glutamate is involved with learned associations (cues) with the drug-taking environment
Glutamate in accumbens –> cravings

41
Q

What happens in the PFC after drug use?

A

The dorsal PFC is active during craving as inhibiting dPFC neurons reduces craving
Inhibiting the PFC inhibits its release of glutamate in the accumbens thus diminishing cravings
Inhibition of dPFC neurons is important for the control of behaviour

42
Q

How do we incorporate the brain circuits for drug use?

A

Inhibitory control by PFC is ignored or overridden
The info processing is incorrect now, the executive ctrl is now maladaptive
Increased drug/cue saliency (NA, OFC, Hipp ‘feels good’)
Decreased interest in other rewards (NA & OFC)
Loss of control (PFC) - compulsive use (OFC) – Habit (Striatum)
Main neurotransmitters: Dopamine & Glutamate

43
Q

How do coke and amphetamine affect the brain and lead to addiction?

A

Nucleus Accumbens: Sooo good (so unexpected)!
Hippocampus & Amygdala: I remember how good that feels
Dorsal Striatum: It’s a habit!
Prefrontal Cortex: I can’t help it!
Orbitofrontal Cortex: So good and I don’t care about anything else

44
Q

How is the entire brain changed in addiction?

A

“Normal” brain function is replaced by maladaptive brain function
The drive for natural rewards is replaced by the NEED for drug: experience the reward to avoid the discomfort of drug absence
Even when abstinent, cues of drug use produce craving & relapse Addiction is a complex neural disorder

Biopsychology and Learning (15 decks)

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