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Psychology Degree > Addiction & Brain > Flashcards

Addiction & Brain Flashcards

1
Q

What are neurones?

A
  • The building blocks of the central nervous system (CNS)
  • Responsible for receiving, processing and transmitting information throughout the body
  • Roughly 86 billion in the human brain
  • Responsible for cognition, sensory processing, motor control & coordination
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2
Q

What are neurotransmitters?

A
  • Chemical messengers that transmit signals between neurons to other neurons across a synaptic cleft
  • Presynaptic neurone – synaptic cleft – postsynaptic neurone
  • Neuropeptides: (subset of neurotransmitters) typically more complex and have longer lasting effects compared to traditional neurotransmitters
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3
Q

Classic neurotransmitters: 4 examples

A
  • Dopamine - cocaine (reward/excitement)
  • Noradrenalin – cocaine (alertness/excitement)
  • Serotonin - MDMA (happiness/love)
  • Acetylcholine- nicotine (focus/memory)
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4
Q

Drugs & Synaptic transmission

A
  • Agonist: typically involves binding to a receptor and activating it (mimicking a neurotransmitter)
  • Antagonist: typically involves binding to a receptor and not activating it (blocking a neurotransmitter)
  • Autoreceptors: these allow the neuron to self-regulate releasing or not-releasing, so things don’t get flooded (homeostasis)
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5
Q

Evidence of neurochemicals in addiction:
(Gerra et al 2000)

A
  • PRL = prolactin (pituitary hormone)
  • Fenfluramine promotes 5-HT release (used clinically to treat obesity, here to test 5-HT function, 5-HT regulates PRL)
  • Long term: the drug itself is no longer present, but long-term effects are found
  • Issues: little dose knowledge from MDMA users (only 100% in animal studies), people tend to underreport doses
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6
Q

Evidence of stress in addiction:
(Miczek & Mutschler 1996)

A
  • Rats trained to respond for cocaine or food reward
  • ‘Social stress’ = 60 mins as an intruder in the cage of a resident rat (protected from attack by a wire mesh)
  • Issues: cause and effect issues
  • Results: rats sought out cocaine over food once in a stressful situation
  • Suggests selective effects of social stress on cocaine-reinforced responding
  • Clinical reports suggest role of stressful life events in relapse, but these are correlational. Controlled animal studies can show cause and effect
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7
Q

What are catecholamines?

A

Catecholamines:
- They are psychomotor stimulants (e.g. dopamine, noradrenaline, serotonin, acetylcholine)
- Neurotransmitters and hormones derived from the amino acid tyrosine
- They play key roles in the body’s stress response, regulation of the blood pressure, heart rate, and various metabolic processes
- Tyrosine has something to do with dopamine synthesis

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8
Q

Hacking catecholamines

A
  1. A = potential to bond at receptor site
  2. B = full agonist
  3. C = antagonist (drug attaches but no response triggered)
    - Cocaine: inhibits DA & NA transporters
    - Amphetamines: increased DA & NA release
    - Risperidone: blocks DA receptors (used in bipolar/ schizophrenia treatments)
    - Ritalin: blocks DA & NA uptake (i.e. ADHD)
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9
Q

Indirect agonist: 2

A

(Bloomfield et al 2016)
- THC promotes DA release through cannabinoid receptors
- Long term DA system dulling
(Reigel et al 2007)
- Same results
- They are interacting with the systems that interact with dopamine levels

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9
Q

What is reserpine?

A
  • General catecholamine antagonist
  • Inhibits VMAT, a protein responsible for moving them into vesicles
  • Test: injected rabbits with the drug
  • Results: quite dramatic behavioural effects that follow their manipulations when we interfere with these process (e.g. become lethargic)
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10
Q

Dopamine pathways: 4 types

A
  • Neural circuits through which dopamine travels to regulate various physical and psychological functions
  • These pathways are critical for processes like movement, reward, motivation, emotion, and hormonal control
  • A) mesocortical
  • B) mesolimbic
  • C) nigrostriatal
  • D) tuberoinfundibular
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11
Q

Dopamine pathway: Mesocortical

A
  • Regulates cognition, decision-making, emotion, and social behaviour
  • Originates in the ventral tegmental area (VTA) but projects to the prefrontal cortex
  • Dysfunction or underactivity is associated with negative systems or schizophrenia and cognitive impairments
  • Drugs = target the mesocortical dopamine pathway that primarily aim to modulate dopamine activity in the prefrontal cortex
  • These drugs are used to address cognitive dysfunction, ADHD, depression, and schizophrenia
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12
Q

Dopamine pathway: Mesolimbic

A
  • Involved in reward, motivation and the feeling of pleasure
  • This pathway plays a central role in reinforcing behaviours and the development of addiction
  • Originates in the ventral tegmental area (VAT) and projects to the nucleus accumbens and other limbic areas (e.g. amygdala & hippocampus)
  • Overactivity in this pathway is linked to addiction, positive symptoms of schizophrenia and other disorder’s involving reward processing
  • Drugs = target the mesolimbic dopamine pathway primarily aim to modulate dopamine activity in the rewards and motivation system of the brain
  • These drugs are commonly used to trat schizophrenia, addiction, depression, and Parkinson’s disease
  • High dopamine in the mesolimbic pathway = psychosis, addiction, mania
  • Low dopamine in the mesolimbic pathway = depression, anhedonia, apathy
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13
Q

Dopamine pathway: Nigrostriatal

A
  • Controls movement and motor planning by facilitating the interaction between the basal ganglia and other motor control systems
  • Starts in the substantia nigra and projects to the striatum (caudate nucleus and putamen)
  • Degeneration of neurons in this pathway is a hallmark of Parkinson’s disease, leading to tremors, rigidity, and bradykinesia
  • Overactivity can contribute to involuntary movements seen in conditions like tardive dsykinesia
  • Drugs = crucial for motor control and used for Parkinson’s disease, drug-induced movement disorders, and Huntington’s disease
  • Low dopamine = Parkinson’s, drug induced
  • Excess dopamine = tardive dyskinesia, Huntington’s chorea
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14
Q

Dopamine pathway: Tuberoinfundibular

A
  • Regulates in the secretion of prolactin from the anterior pituitary gland, playing a role in hormonal control
  • Originates in the hypothalamus and projects to the pituitary gland
  • Dysfunction can result in hyperprolactinemia, leading to symptoms such as infertility, sexual dysfunction and galafactorrhea (milk production)
  • Drugs = DA acts as a prolactin antagonist
  • Increase prolactin = infertility, menstrual irregularities decreased libido
  • Decreased prolactin = rare and usually not clinically significant unless in conditions like hypopituitarism
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15
Q

How do we target drugs?

A
  • DA has multiple receptors (e.g. multiple locks work for the same key)
  • Some activate easily (D3), and others less so (D1)
  • Some excite the neuron (D1-like), while others calm in down (D2-like)
  • Location in different regions (e.g. D1 is key for motivation and movement, while D3 is more involved in addiction and impulse control)
16
Q

Beyond drugs: 2 studies

A

(Giros et al 1996)
- From birth, not CRISPA edited
- Heterozygous = 1 deletion
- Homozygous = double deletion
- ABOVA shows double deletion = more active. The dopamine transporter would usually remove the dopamine
- An animal under treatment to become more hyperactive will respond by wanting more of that treatment, suggesting its rewarding and showing addicting potential
(Xu, Guo, Vorhees & Zhang 2000)
- Mutant mice lacking D1 receptors are insensitive to cocaine which increased locomotor activity in the wild-type but not the knockout mice

17
Q

Patterns of drug use: Past

A

According to earlier British Crime Surveys (BCS):
- In 1996, around 30% of adults had tried illegal drugs at some point in their lives
- In 1998, this increased slightly to around 32%
- By 2000, it was around 33% (1 in 3 adults)

18
Q

Patterns of drug use: Now

A
  • UK: 38% of adults aged 16-59 have tried drugs
  • USA: the national survey on drug use and health 2022 reports that over 50% of adults aged 12+ have tried an illicit drug at some point in their lives
  • UK 2024: 8.8% of adults (16-59) reported using drugs
  • USA 2022: 17.3% of Americans 12+ using illegal drugs
19
Q

Key facts of drug use

A
  • Drug use is relatively stable overtime
  • Most illicit drug isn’t daily
  • Most drug use is by younger people
  • Most drug use is by less affluent people
  • Most drug use is by men
  • Use patterns vary by drug and age
  • PCP (e.g. angel dust a dissociative anaesthetic)
  • Salvia (herb in Mexico that produces hallucinogenic experiences)
20
Q

Exposure models: Key features

A
  • Most models of addiction are exposure models
  • All people are at risk of becoming addicted to drugs given sufficient exposure
  • Drugs interact with and change the brain
  • Brain changes create continued motivation to use the drug
  • Models differ in their explanation as to what sort of changes drugs produce in the brain and what sort of motivation drives subsequent drug use
  • Focus on withdrawal
21
Q

Withdrawal: key features

A
  • Addicts continue to use the drug to avoid withdrawal
  • The initial high exhausts the reward/pleasure regions of the brain and once the drug wears off the user goes into withdrawal (VERY aversive)
  • A form of negative reinforcement
22
Q

Withdrawal model issues: Relapse

A
  • Stopping drugs under medical supervision does not necessarily result in long term abstinence
  • Drug users often relapse despite having undergone supervised withdrawal from drugs
  • Wikler (1948) proposed that withdrawal can be triggered by external cues
  • Environmental stimuli such as the addict’s bedroom is consistently paired with withdrawal
  • Through pavlovian conditioning, stimuli enter learned associations to become triggers for withdrawal symptoms
  • Subsequent exposure to these cues is then sufficient to elicit withdrawal and thereby precipitate relapse
  • Thus, conditioned withdrawal can explain relapse following primary withdrawal
  • Anecdotal reports from relapsed drug users suggest things are not always as predicted e.g. by contexts in which withdrawal had occurred most frequently
  • People can associate cues with outcomes over a delay or a trace (lingering effect of drugs)
23
Q

Withdrawal model issues: can’t all be aversive

A
  • Midbrain dopamine cells increase activity when humans or animals detect or consume both natural rewards (food, water, sex) and drugs of abuse (nicotine, cocaine, heroin)
  • Suggest that drugs of abuse hijack the brain substrate for reward/pleasure and are consumed because drug taking is positively reinforcing
24
Q

Opponent process model

A
  • Initial positive experience – positively reinforcing drug use
  • Subsequent negative experience – where the body attempts to restore balance, leading to a negative effect (withdrawal)
  • With repeated use – the initial positive effects become weaker (tolerance) and the negative effects become stronger
  • CREATES A CYCLE OF ADDICTION
  • Solomon & Corbit (1973) – sky divers feel a mixture of fear and pleasure but after multiple jumps they start to be less afraid and more excited (relates to drug use – pleasure decreases & withdrawal increases overtime)
25
Q

Tolerance: 2 types

A
  • Pharmacodynamic tolerance: this occurs when the drug’s effects at the cellular or receptor level become less pronounced
  • Pharmacokinetic tolerance: this arises when the body becomes more efficient at metabolising or eliminating the drug (e.g. drinking)
26
Q

Conditioned tolerance: Siegel (1983)

A
  • High heroin dose given to heroin tolerant rats
  • Deaths by environment (Novel – 96%, Usual – 64%)
  • Environmental cues associated with drug taking can elicit a ‘drug opposite’ response
  • Drug opposite response may be aversive, and motivate drug taking to alleviate this state (negative reinforcement
27
Q

Positive condition: Hogwarth et al (2010)

A
  • Data consistent with hypothesis drug cues prime drug taking by reminding the addict of the positive appetitive qualities of the drug (not by eliciting an aversive state)
28
Q

Exposure vs susceptibility models

A
  • Exposure models – addiction is caused by the drug and the neurological changes it promotes (withdrawal, opponent process)
  • Susceptibility models – addiction is caused due to individual vulnerabilities such as genetic, psychological to environmental factors (more people are more susceptible to drugs than others & not everyone becomes an addict)
29
Q

Susceptibility factors: 3 main factors

A
  1. Age – peak time with drugs is typically from late teens to early 20s
  2. Sex - men are more susceptible to drugs
  3. Genetics – research suggests that 40-60% of addiction vulnerability is hereditary.
    Specific genes affect how individuals respond to substances and their likelihood of developing addictive behaviours (e.g. fewer dopamine receptors or increased metabolism). BIG issues with nature vs nurture
  4. Other factors include drug availability, broken home, mental health of parents, failure at school & role modelling (BUT problems with disentangling cause and effect)
30
Q

Susceptibility factors: Tarter et al (2003)

A
  • Longitudinal study with children from age 10 to 19
  • Split into high and low-risk groups
  • Matched across household income, parent education, parent use, etc
  • Concluded that ‘Neurobehavioral disinhibition’ was greater in the high-risk group and predicted illicit drug use
31
Q

Neurobehaviour disinhibition

A
  • a composite source of (difficult temperament, ADHD, depression, low cognitive function). Those at risk of drug abuse show disorganised behaviour, possibly stemming from abnormality in the frontal cortex, causing poor decision making
  • Phineas gage (1823-1860): accident cause a large railroad spike to impale his head, causing a SEVERE frontal lesion. Become unreliable at work, showed callous regard. Preserved some intellectual function (e.g. memory), but planning ability become very poor. Became an alcoholic and hyper-sexual
  • Conclusion: suggest PFC associated functions, such and decision making, long-term thinking, self-control, impulsivity and risk-taking tendencies influence addiction behaviour
32
Q

Iowa gambling task & risky decision making

A
  • 4 decks of cards with a goal to win money
  • Participants told all cards result in some level of reward
  • Occasionally, choosing a card causes them to lose some money
  • A & B are ‘bad decks’, C & D are ‘good decks’ but they are rigged
  • Most people can figure it out that the cards are rigged but addicts can’t figure this out
  • Bechara et al (2000) – patients with PFC lesions do worse than normal because they opt for high immediate gains despite higher future loses
  • Deakin et al (2004) – general impression is that maturity increases over age until 20/25. Suggest the susceptibility for drug use amongst younger people might be due to PFC underdevelopment
  • In the Iowa gambling task, who frequently selects the high reward desks despite the net loss of points include (with frontal lesions, in adolescence, ADHD, schizophrenia, drug addicts)
33
Q

Cause and effect: risky decisions, drug use and PFC damage

A
  • Risky decision making seen in high-risk children before any drug use
  • Risk decision making predicted the onset and magnitude of drug use
  • Suggests PFC damage is a major susceptibility factor for becoming a drug user
  • several aspects of risk decision making can predict drug use (reward hypersensitivity, reward hyposensitivity, punishment insensitivity, faulty error detection)
34
Q

Punishment insensitivity: clinical relevance

A

DSM drug dependence criteria:
1. continued use of drugs even though known to cause trouble with family/friends
2. job troubles because of drug use
3. continued use of drugs even though known to cause health problem
- Test: trained rats to give themselves coke then put them through withdrawal. reintroduced coke and provided a cue that previously predicted coke delivery, some relapsed. introduced a small experiment punishment (small shock) for relapsed rats
- Results: some animals keep wanted the coke EVEN WHEN paired with a shock

35
Q

Error detection: control vs drug addicts

A
  • addicts may have full knowledge of the adverse consequences of their drug taking, but just not able to sue this knowledge to correct their behaviour
  • event related potentials (ERP) used to measure the responses of cocaine addicts to errors in their performance
  • Flanker test: cocaine addicts showed a reduced frontal activity in response to errors and less post-error improvement in performance
  • suggests that addicts may have less knowledge of the adverse consequences of their behaviour, and so less ability to use this knowledge to modify their behaviour
  • controls show sensitivity in the PFC when they make an error, but coke addicts don’t

Psychology Degree (13 decks)

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