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PSYCHOLOGY - semester 2 > Addiction and the Brain > Flashcards

Addiction and the Brain Flashcards

1
Q

what are neurons?

A

A nerve cell, building blocks of the CNS, they receive, process and transmit info throughout the body

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2
Q

what are neurotransmitters?

A

They are chemical messengers that allow neurons to communicate with each other

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3
Q

what is dopamine?

A

DA: is a classical neurotransmitter, often referred to as “feel good” due to its involvement in the reward system.

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4
Q

what is the association of amphetamines and cocaine to dopamine?

A

They have an impact on dopamine neurotransmission, cocaine blocks dopamine reuptake and amphetamines increase dopamine release

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5
Q

what is nonadrenalin?

A

NA: is a classical neurotransmitter involved in the bodys “fight-or-flight” response. plays a role in alertness and arousal/excitment

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6
Q

what is the association of amphetamines and cocaine on nonadrenaline?

A

they both affect the levels in the brain, amphetamines can increase the release from neurons, and cocaine can block reuptake leading to a buildup in the synaptic cleft = amplifying fight or flight response and can lead to addiction

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7
Q

what is serotonin?

A

5-hydroxytryptamine, 5-HT: is a classical neurotransmitter associated with happiness and love

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8
Q

what are the effects of ecstasy on serotonin?

A

effects of levels in the brain: increased serotonin release, leading to depletion of stores in brain leading to depression etc

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9
Q

what is acetylcholine?

A

ACh: is a classical neurotransmitter associated with focus, learning and memory

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10
Q

what are the effects of nicotine on acetylcholine?

A

nicotine acts as a stimulant by mimicking ACh, binds to nicotinic ACh receptors which stimulates the release of varieous neurotransmitters, over times changes sensitivity of ACh receptors = desensitisation

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11
Q

What is a agonist?

A

+ Is a substance that binds to a specific receptor and activates it, mimicking the action of a natural ligand (neurotransmitter)

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12
Q

What is an Antagonist?

A
  • is a substance that binds to a specific receptor but blocks the action or the natural ligand or other agonists
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13
Q

What is an autoreceptor?

A

:is a type of receptor located on the presynaptic neuron thast sensitive to the neurotransmiiter that the neuron itself releases, allowing the neuron to self-regulate releasing or not releasing to prevent flooding

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14
Q

What are catecholamines?

A

:Are a group of neurotransmitters and hormones known for their role in the body stress response (regulation of blood pressure, heart rate and metabolic processes), they’re derived from the amino acid tyrosine

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15
Q

what are the two main neurotransmitter examples of catecholamines?

A

dopamine and nonadrenaline

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16
Q

what is the effect of risperidone on dopamine?

A

is an atypical antipsychotic medication, which blocks DA receptors in the brain, used in schiz and bipolar treatment

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17
Q

what are the effects of ritalin on DA AND NA uptake?

A

Ritalin (methylphenidate) is a stimulant medication used to treat ADHD/narcolepsy/sleep disorder. it blocks DA + NA uptake = ends up w/ more dopamine

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18
Q

what is RESERPINE?

A

is a general catecholamine antagonist, inhibits VMAT - a protein responsible for depleting stores of some neurotransmitters to cause sedation, depression etc - used to treat schiz + anxiety etc

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19
Q

what are indirect agonists?

A

: a substance that enhances the action of a neurotransmitter but doesnt directly bind to the neurotransmitter receptor itself

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20
Q

How is cannabis an example of an indirect agonist?

A

: not chemically/directly related to dopamine system, but THC promotes DA release through cannabinoid receptors, long term use causes DA system dulling

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21
Q

what are dopamine pathways?

A

They are neural circuits through which dopamine travels to regulate various physical + psychological functions. These are critical for process like movement, reward, motivation, emotion and hormonal control

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22
Q

What is the Mesocortical dopamine pathway?

A

: originates in the ventral tegmental area, but projects to the pfc and regualtes cognition, decision-making, emotion and social behaviour. dysfunction/underactivity is associated w/ negative symptoms of schiz

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23
Q

what drugs are used to target the mesocortical dopamine pathway and why?

A

risperidone which promotes DA in the PFC, are used to reduce symptoms of apathy, lack of motivation and cognitive impairments etc

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24
Q

What is the mesolimbic dopamine pathway?

A

: originates in the ventral tegmental area and projects to the nucleus accumbens + other limbic areas (amygdala/hippocampus), its involved in reward/ motivation + feeling of pleasure so plays role in reinforcing behaviours and the development of addiction

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25
what does overactivity/underactivity in the mesolimbic dopamine pathway cause?
overactivity causes (high dopamine) is linked to addiction, positive symptoms of schiz (mania), underactivitiy (low dopamine) is linked to depression, anhedonia, apathy
26
why are drugs used to target the mesolimbic dopamine pathway?
aim to modulate dopamine activity in the reward and motivation system of the brain, they are used to treat schiz, addiction, depression and parkinsons disease
27
what is the nigrostriatal dopamine pathway?
this is a smaller pathway which starts in the substantia nigra and projects to the striatum and controls movement and motor planning by facilitating the interaction between the basal ganglia and other motor control systems
28
what does degression/ overactivity of the nigrostriatal dopamine pathway cause?
Degression of neurons (low dopamine) in this pathway can cause parkinsons disease - leading to tremors, rigity, - Overactivity (excess dopamine) in the area can cause involuntary movements seen in conditions like tardive dyskinesia
29
why are drugs used to target the nigrostriatal dopamine pathway?
drugs are used for motor control, treats parkinsons, drug induced movement disorders and huntingtons disease
30
what is the tuberoinfundibular dopamine pathway?
: originates in the hypothalamus and projects to the pituitary gland which is associated with hormone release, it regulated the secretion of prolactin from the anterior pituitary gland, playing role in hormonal control
31
what can dysfunction in the tuberoinfundibular dopamine pathway cause?
can result in the hyperprolactimenia, leading to symptoms such as infertility, sexual dysfunction, and galactorrhea (milk production)
32
what is the role of dopamine in the tuberoinfundibular dopamine pathway?
dopamine acts as a prolactin (hormone) antagonist, increased prolactin causes infertility, decreased is rare and there arent signf consequences
33
what are the different dopamine receptors and how are these used to target drugs?
there are D1-5, these are multiple locks fro the same key and are located in different regions, some activate easier (D3- involved inaddiction + impulse control), some not so much (D1- involved in motivation + movement), some excite the neuron (D1-like), while others calm it down (D2-like)
34
how did the results of the British crime surveys change from 1996 to 2000?
in 1996, 30% of adults had tried illegal drugs, this increased to 33% by 2000
35
what were the results of the national survey of drug use and health in 2022 show about Americans?
reports that over 50% of Americans aged 12+ have tried an illicit drug at some point in their lives
36
what are Exposure models of addiction?
:theoretical frameworks - attempt to explain how repeated exposure to addictive substances or behaviors can lead to the development of addiction, all ppl are at risk given sufficient exposure. also that drugs interact + change the brain which create continued motivation to use the drug
37
what is the exposure models explanation of withdrawal?
addicts experience withdrawal when the initial high exhausts the reward/pleasure regions of brain and the drug wears off, it is very aversive. this is negative reinforcement as addict conts taking substance to remove withdrawal symptoms
38
what is the issue with the withdrawal model explanation proposed by conditioned withdrawal?
there are consistent pairings with withdrawal such as an addicts bedroom, which enters into learned associations to become triggers for withdrawal symptoms. if one is exposed enough to these cues, relapse could be triggered
39
what are inhalants?
inhalants are a type of psychomotor stimulant, they're 'volatile; liquids/gases that readily vaporize. Also they're a diverse range of compounds with wide-ranging effects
40
what are the 3 types of inhalants?
1) volatile solvents: liquid at room temp, give off fumes 2) aerosols: contain solvents/ propellants 3) gases: can be sniffed/inhaled/sprayed into the mouth
41
what are the behavioural effects of acute exposure to inhalants?
euphoria, disinhibition, stimulation then lightheadedness, drowsiness (like alcohol)
42
what are the behavioural effects of heavy exposure to inhalants?
slurred speech ataxia, lethargy, hallucinations, sometimes delusion
43
what are the behavioural effects of very high doses of inhalants?
anaesthesia, coma
44
what was the original use of inhalants?
use dates to early human history related to mystical practices where spiritual leaders inhaled fumes from incense, oils or perfumes to alter consciousness
45
who was Sir Humphry Davy?
british scientist popularized nitrous oxide, cheap substitute for alcohol, who held NO parties and coined th eword "laughing gas" in 1799
46
how are the effects of inhalants mediated in the brain?
theyre rapidly absorbed, so theyre fat soluble. its distributed widely around the brain - especially the striatum, thalamus and deep cerebellar nuclei
47
why are inhalants addictive
dopamine is the substrate of normal reward systems, and is a common factor across a broad spectrum of addictive drugs. the Mesolimbic pathway also is implicated in natural reward and drugs abuse (the dopamine pathway responsible for rewards, motivation and emotions)
48
what is the evidence that the mesolimbic pathway is activated when consuming inhalants (such as toluene)
Anaesthetized rats - toluene and measured firing in ventral tegmental area (VTA: Riegel and French 1999)
49
what is funada et al (1992) evidence for why inhalants are addictive?
study on mice - placed in 2 connected chambers and toluene distribueted into only one. exposed rats show + locomotor activity and reduced anxiety behaviour and preference for toluene chamber = suggesting has stimulating effect on CNS and change in levels of neurotransmitters
50
why are inhalants reinforcing?
the same brain areas are activated in response to toluene as alcohol, opiated and cannabis: 1) .. Inhalants enhance function of GABA and glycine inhibitory receptors 2) Inhalants inhibit excitatory NMDA glutamate receptors (like ketamine) = similar to alcohol - reduce CNS excitability
51
what are the short term effects of chronic inhalant use?
- Slurred speech - Runny nose/bleeds - Tiredness - Ulcers or irritated nose + mouth
52
what are the long term effects of chronic inhalant use?
- Confusion - Poor conc - Depression - Irritability - Hostility - Paranoia NEUROLOGICAL DAMAGE: cause permanent damage to the NS, leading to conditions such as peripheral neuropathy an encephalopathy RESPITORY ISSUES: inhaling can irritate respiratory tract and lead to chronic respiratory problems CARDIOVASCULAR PROBLEMS: can result in irregular heart rhythm and increase the risk of sudden cardiac arrest
53
what is sudden sniffing death syndrome?
SSDS can be caused from use of inhalants, leading to sudden rapid heart rhythms or irregular heart rhythms
54
what is deadly blood disorder (methemoglobinemia)?
can result from inhaling nitrates or poppers which is where the blood becomes physically changed so that is cant deliver oxygen to the body
55
what are the legal issues surrounding inhalant use/being sold?
- Under Scottish law you can be prosecuted for 'recklessly' selling substances to any age group if you suspect they're going to inhale them Since october 1999, the law makes it an offence to supply gas lighter refills to under 18s, law applies to whole of UK
56
what is gamma hydroxybutyrate? (GHB)
a type of psychomotor stimulant which is a natural product of human metabolism, carb found in our diet (meat,wine etc) and also biologically synthesised from GABA - an amino acid that is structurally similar to GHB. = a naturally occurring neurotransmitter in the central nervous system and a depressant drug
57
what is Gamma-hydroxybutyrate (GHB) used for?
they're used clinically to treat cateplexy (sudden loss of muscle control experienced by narcoleptics), narcolepsy and alcohol dependency. often misused for its psychoactive effects
58
what are the behavioural effects of lower doses of GHB? (gamma hydroxybutyrate )
Euphoria Relaxation and Tranquility Increased Sociability Increased Libido   Disinhibition
59
what are the behavioural effects of higher doses of GHB? (gamma hydroxybutyrate )
Drowsiness and Sedation Dizziness   Loss of Coordination (ataxia)   Nausea and Vomiting Memory Impairment   Hallucinations Unconsciousness and Coma Respiratory Depression Seizures Death
60
how quickly and for how long do the effects of GHB (gamma hydroxybutyrate) come on and last for?
The effects typically felt within 15 mins and last for around 3-4 hours
61
what are the 3 forms GHB (gamma hydroxybutyrate ) can come in?
1) a colourless, odourless, bitter or salty-tasting liquid – sold in small bottles or vials 2) a blue coloured liquid 3) crystals or powder (this is less common).
62
what is the interaction between ghb and gaba?
ghb acts as a weak agonist at gaba receptors which are the primary inhibitory receptors in the brain. = explains depressive effects
63
what is the effect of ghb on dopamine?
Dopamine associated with most drugs and leads to reinforcement. Targets the mesolimbic pathway, induced a sense of reward through dopamine release, thus becomes reinforcing.
64
what is: The GHB Receptor Hypothesis?
one of the main hypotheses regarding the neural mechanisms of GHB: - ghb effects are mediated by a specific ghb receptor - high density found on hippocampus and cerebral cortex
65
what is the: The GABA<0xE2><0x82><0x90> Receptor Hypothesis?
one of the main hypotheses regarding the neural mechanisms of GHB: - ghb mediated pre/post-synaptic gaba release - GHB acting as a weak agonist at the GABA receptor
66
what are the consequences of long term use of ghb (gamma hydroxybutyrate)?
Can lead to: - severe memory problems - heart disease - Hallucinations - extreme anxiety - breathing problems Some evidence from rats that long term exposure can lead neurological damage, affecting the 'grasping' reflex, as well as alteration in spatial and working memories (pedraza et al 2009)
67
what is zeng et al 2022 research on the adverse effects of ghb usage?
ppts were slower on behavioural tasks that other addicted groups and healthy controls - Particularly bad at visuospatial, executive function, and memory tasks. - showed signf decrease in areas of all lobes and central area
68
what are the withdrawal symptoms of ghb?
symptoms reported as insomnia, anxiety and tremors, and at high doses even hallucinations, delirium, extreme agitation and psychosis
69
what % of children in th eus have tried inhalants by 4th grade?
6%
70
what is the issue in australia with inhalants and how have the combatted the issue?
long standing issue with petrol sniffing in indigenous communities = some areas using non-sniffable fuel called opal
71
what has south africa reduced to keep kids safe from inhalants?
after reports of some being left paralyzed from glue sniffing, glue manufacturer greatly reduced the n-hexane content in their glue products
72
what has been found of the effects of ghb on nacolepsy?
EDS is the most common symptom seen in narcolepsy - causes persistent sleepiness and sudden "sleep attacks" despite getting enough sleep at night - A systematic review and meta-analysis found ghb was effective in treating EDS and cataplexy, though th medication was also not well tolerated (xu et al 2019)
73
what is the difference between anabolic and androgenic steroids?
Anabolic: increase muscle mass Androgenic: masculinising/testosterone-like
74
what are steroids (simply) ?
Essentially it is a largely synthetic testosterone - May be used therapeutically to treat condts like low t/hypogonadism in males - Also used therapeutically e.g. for rheumatoid arthiritis and anaemia and to build muscle for the bed ridden
75
who was brown-séquard in the context of steroids?
- In the 1870’s Brown-Séquard began his experiments with testicular extracts, suggesting some form of chemical/ hormonal understanding - Testosterone was isolated in the 1930s, and numerous synthetic androgens were quickly developed thereafter
76
in the 1900s, when did steroids begin to be used and for what?
- By the 1940s - benefits of the drugs muscle gain for athletic purposed became realised - By the 1950s the drug was being used by doctors overseeing body builders and widely used by Russian weightlifters and then began to move into other sporting events
77
in 2016 what happened to all russian weightlifters?
were banned from the olympics with doping being so prevalent
78
what are the ways in which steroids can be taken in athletes?
Steroids taken orally or intramuscularly, also in creams/gels or as patches
79
what does of steroids do endurance athletes/sprinters take compared to body builders?
Endurance athletes and sprinters use low doses, Bodybuilders and strength athletes use up to 100x therapeutic dose
80
what is the problem with oral steroids?
Oral steroids potentially metabolised too fast in liver to act
81
what has been done to overcome the problem of rapid metabolism of steroids?
Additional variants specially designed to avoid problem of rapid metabolism, and to minimize androgenic relative to anabolic effects
82
what are the effects of androgenic steroids?
- psychological effects of 'male' characteristics (aggression etc) - development + maintanence of libido - pubertal voice alterations - increased hair
83
what are the effects of anabolic steroids?
- increased skeletal muscle mass - improved T-lymphocyte production - increased size of organs - retention of electrolytes - altered distribution of body fat
84
what is the hypotheses that steroids act at androgen receptors?
explains effects of steroids, saying androgen receptors are present in cytoplasm of muscle, androgen binds, activation increases protein synthesis and muscle growth
85
what is the issue with the hypotheses that steroids act at androgen receptors?
Some argue that normally androgen receptors already saturated - so how can steroids work on them?
86
what are the 2 alternative hypotheses that avoid the issue of androgen receptors being already saturated so steroids cant work on them?
Hypothesis 2: steroid treatment induces receptor expression in muscle Hypothesis 3: androgens are antagonists for glucocorticoid hormones - which are catabolic: decrease protein synthesis, increase in protein breakdown
87
what are common behavioural side effects of chronic steroid use?
The following are reported in steroid users (meeting DSM criteria) - take more than intended - can't cut down even though want to - spend much time obtaining and using - continue use despite problems use causes - replace other activities with substance use
88
what are the withdrawal symptoms of chronic steroid use?
fatigue, Depression, insomnia, restlessness, anorexia, decreased libido, dissatisfaction with body image, desire for more steroids
89
what is the explanation for the dependence people gain for steroids?
because steroids arent psychoactive and dont produce euphoria or elicit cravings during withdrawal, perhaps initial reinforcement because of effect on body image
90
what are the possible health consequences of anabolic steroid use?
hypertension, incr blood clotting, incr red blood cells, decreased HDL cholesterol, jaundice, tumors, severe acne
91
what are the behavioural effects of anabolic steroid use?
increased libido, irritability and aggressiveness, dependence
92
what are the behavioural effects specific on men of anabolic steroid use?
testicular shrinkage, reduced sperm counts and possible infertility, prostate enlargement, gynecomastia (breast growth)
93
what are the behavioural effects specific on women of anabolic steroid use?
menstual abnormalities, deepening of the voice, excessive hair growth, especially on face, enlargement of the clit, decreased breast size
94
who is professor david nutt and what were his opinions on steroid use?
chairman of the council's technical committee said It had been estimated that there were tens of thousands of people using steroids to improve the results of training regimens to make themselves look more muscular.
95

PSYCHOLOGY - semester 2 (3 decks)

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