Substance abuse Flashcards

Question

Prolonged use of meth can lead to what?

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

* 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

Answer 6

* 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

Answer 7

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

Answer 8

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

Answer 9

* Anxiety * Depression * Psychosis May be treated with available pharmacotherapies Pharmacotherapies for addiction arent good

Answer 10

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

Answer 11

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

Answer 12

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)

Answer 13

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

Answer 14

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

Answer 15

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

Answer 16

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

Answer 17

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

Answer 18

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

Answer 19

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

Answer 20

“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