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PSY290: Behavioral Neuroscience > Week 9: Drugs and Substance abuse > Flashcards

Week 9: Drugs and Substance abuse Flashcards

1
Q

Drug

A

Chemical substance that produces biological effect when ingested. Can be natural or synthetic, not a vital nutrient

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2
Q

Uses for drugs

A

Context is key; can have good and bad effects
Good = therapeutic uses
Bad = unwanted drawbacks or perceived risk

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3
Q

How drugs are categorized

A

Weighing the benefits vs. the risks. All drugs cause harm in some capacity

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4
Q

Change of drug attitudes over time (Examples)

A

Cannabis has become more normalized
Cocaine, amphetamines, and opioids are no longer used in everyday OTC medicine

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5
Q

Desired effect of a drug

A

The therapeutic effect sought

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6
Q

Side effects of a drug

A

Any unwanted effects other than the therapeutic use

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7
Q

Relationship of dose and effect

A

As dosage increases, magnitude of effects increases

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8
Q

Dose-Response Curve (DRC)

A

Measurement of relationship between dose and behavioral response. Dose on x-axis, percent of population with a response on y-axis

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9
Q

Effective dose 50 (ED50)

A

Dose where 50% of the population shows the desired effect. Dose amount may very based on drug type

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10
Q

Toxic dose 50 (TD50)

A

Dose where toxic effects occur in 50% of the population.

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11
Q

Therapeutic window

A

Difference between the ED50 and TD50. Want this difference to be as large as possible

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12
Q

Repeated use effects on DRC

A

The dose-response curve will move with repeated use as tolerance builds

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13
Q

Routes of administration

A

Oral, intravenous, intramuscular, subcutaneous (below the skin)
Route type determines speed of effects kicking in and amount of drug in the bloodstream
IV hits fastest and hardest; oral and subcutaneous are slower and weaker

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14
Q

Drug effect curve

A

The measurement of when and how much drug effects will occur takes a curve shape.

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15
Q

Risks and benefits of administration routes

A

Every route has risks. Oral is the least risky, and epidural is the most risky, but has the fastest and largest payoff

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16
Q

Blood-brain barrier

A

Blocks certain drugs from ever reaching the brain (like dopamine). Requires transport facilitation to pass.

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17
Q

Role of individual differences in drug use

A

Many factors can change the way drugs effect somebody, like environment, genetics, etc.

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18
Q

Alcohol metabolism genetic variation

A

The aldehyde dehydrogenase (ALDH) and alcohol dehydrogenase (ADH) enzymes may vary, and those with variations cannot metabolize alcohol. Genetic guarantee of no addiction to alcohol

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19
Q

CYPD2 Enzyme variation

A

Related to the metabolism of many drugs, and if it’s altered response to many drugs can change predictable

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20
Q

Mechanisms of drug action

A

Can act on affecting transporters or can interact with other drugs. Acts as an agonist (excitatory) or antagonist (inhibitory)

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21
Q

Example of transport affect in drug use

A

Cocaine inhibits dopamine transports which keeps dopamine in the synapse longer, allowing more to be taken in by receiving cell

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22
Q

Example of drug to drug interactions

A

Alcohol and benzos superactivate the GABA system

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23
Q

Ways to classify drugs

A

Chemical structure, behavioral effects, biological effects, legal status, etc. Organizing by one will create something similar to the other categorizations
Class definition: a drug is anything that affects mood or behavior, can be used to treat illness, and has the capacity to be abused

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24
Q

Anti-anxiety agents and sedative-hypnotics

A

Reduce anxiety, cause sedation or induce sleep. Increases GABA system activity; low dose therapeutic window.
Benzos, alcohol, GHB, anesthetics, ketamine

25
Q

Antipsychotic agents

A

Treats psychosis/disconnection from reality. Inhibits Dopamine 2 Receptors. Invention reduced rates of lobotomy and institutionalization
Gen 1: chlorpromazine and Haloperidol
Gen 2: Clozapine
Long term effects: impaired movement and weight gain

26
Q

Antidepressants and mood stabilizers

A

Treat mood disorders and bipolar. Monoamine Oxidase Inhibitors (MOIs) block break down of monoamine
Tricyclic antidepressants and SSRIs affect serotonin and noradrenaline transport

27
Q

Opioid Analgesics

A

Act on opioid receptors to reduce pain. High risk for tolerance, addiction and withdrawal

28
Q

Psychotropics

A

Drugs that affect the mental state. Very broad category, fits almost all drugs.

29
Q

Psychadelics

A

Psilocybin and LSD, potential therapeutic uses are currently being studied

30
Q

Microdosing psychadelics

A

Taking amounts smaller that the dose needed to experience hallucinations, but will get enhancing effects. Not empirically supported, but being researched

31
Q

Tolerance

A

Reduction of effect over time with repeated drug use. Can be reversed if you abstain from the drug for a long period of time.

32
Q

Mechanisms for tolerance (3)

A

Metabolic = easier metabolizing of drug
Pharmacodynamic = change in how cells respond to drug
Behavioral = learning to mask side effects of drug use

33
Q

Cross-tolerance

A

Use of one drug leading to tolerance of another drug. Ex: benzos and alcohol; both target GABA system, so use of one will limit effects of another

34
Q

Environmental cues for tolerance

A

When using a drug in the same environment, it becomes a cue for the drug and the body will prepare for the drug, thus larger doses will need to be taken to feel the effect. Leave this environment, lose the tolerance, higher risk of overdose

35
Q

Mouse test for environmental cues

A

Injected alcohol in a specific environment and tracked body temperature. Found that any changes in body temperature did not translate to the new environment, but were cued by the location

36
Q

Contingent drug tolerance

A

Tolerance to effects requires direct experience of the effects.

37
Q

Contingent tolerance study

A

Method: Gave two groups alcohol (anti-convulsive) before or after shock treatment.
Findings: The before group developed a tolerance, the after group did not. The effectiveness of alcohol as an anti-convulsive reduced over time for the before group
Suggests that the effects need to be felt for the tolerance to build. The after group never felt the anti-convulsant effects of the alcohol, so they never built a tolerance to it

38
Q

Withdrawal

A

Removing the drug from a system that has now adapted to having the drug

39
Q

Sensitization

A

Increase in drug response over time
Ex: amphetamine induced locomotor sensitization

40
Q

Difference between use disorder and drug dependence

A

Substance abuse requires impairment to day to day function, pervasive thoughts and behaviors surrounding the drug, and cravings for the drug

41
Q

Risk factors for addiction

A

Unstable home environment, early use, lack of education employment status, genetics, gender, and mental health comorbidity (ADHD is the highest)

42
Q

Dysfunction in mood, affect and personality systems theory

A

Prefrontal cortex and amygdala are the driving factors of addiction, and personality is related to drug use

43
Q

Reward system dysfunction theory

A

Prefrontal cortex, striatum and dopamine neurons are driving factors of addiction Argument is that there is a system in the brain which attributes reward and changes motivational drive

44
Q

Neural reward system

A

The mesolimbic pathway, specifically the synapse between the ventral tegmental area (VTA) and the nucleus accumbens (NAC). Dysfunction here contributes to habit formation

45
Q

Role of nucleus accumbens

A

Key role in liking behavior; contains hedonic hotspots of neurons, responsive to drugs, small brain area associated with liking a drug

46
Q

The dopamine hypothesis of addiction

A

Addiction is driven by dopamine release in the reward system. The reward of dopamine drives behavior to continue using the drug

47
Q

Evidence for the dopamine hypothesis

A

Stimulation of dopamine receptors is reinforcing
Antagonism of dopamine prevents self-administration
Rewards and cravings accompanied by Dopamine release
Abnormal dopamine transmission is common in drug users

48
Q

Feedback model of long term drug use

A

Ventral tegmental area strongly activates nucleus accumbens via dopamine when the drug is used. With increased use, NAC will form VTA inhibitors. This may cause a disliking of the drug over time

49
Q

Issues with dopamine hypothesis

A

All human evidence is correlational; best evidence comes from drugs that affect dopamine specifically; dopamine release of drug doesn’t predict addictive properties

50
Q

Cognitive control dysfunction theory

A

Prefrontal and orbitofrontal cortex are key; difficulty in regulating behavior causes addiction

51
Q

Role of frontal cortex

A

deciding to act on drug cravings, inhibiting negative response to drug wanting

52
Q

Role of orbitofrontal cortex

A

Lowered OFC activity associated with less ability to assess value and control behavior

53
Q

Issues with using animal models to test substance abuse

A

Animals lack the rich social environment humans do, and thus lab may not bring the most generalizable results

54
Q

Rat park study

A

Put rats in a rich social environment. Found that rates of drug use in the rats lowered. Suggests lab scenarios don’t mimic the real world

55
Q

Choice vs. disease perspective

A

Choice: personal accountability for actions, reinforcing good behavior
Disease: deficits in biological brain systems
Diff views affect treatment, legal regulation, and social stigma/pressure

56
Q

Theories of addiction (4)

A

Physical dependence = take drug to avoid withdrawal
Positive incentive = take drug for pleasurable effects
Instrumental/self-medication
Personality-based = some traits are positively correlated with drug use

57
Q

Treatment vs. drug type

A

Treatment varies based on drug type, but all addiction is treatable. Biggest issues are access to treatment and social stigma.

58
Q

Types of treatment for addiction

A

Therapy, drug replacement (nicotine patches), or antagonizing the drug effect (med that makes you vom if you have alcohol)

PSY290: Behavioral Neuroscience (10 decks)

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