Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Drugs and Behavior 345A > midterm #2 > Flashcards

midterm #2 Flashcards

1
Q

operationalization of stimulants:
biological (3)
behavioural (4)

A

biological:

  • substance raising levels of physiological activity in the body
  • objective
  • sympathomimetic (cause physiological arousal, suppress parasympathetic nervous system)

behavioural:

  • substance temporarily improving mental/physical function
  • subjective
  • improvement depending on functionality
  • James-Lange theory: attribution can change interpretation (panic vs. happy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

state-dependent memory

A

when memory eretrieval is more accurate under the same conditions as memory encoding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

speed/accuracy tradeoff with stimulants

A

new behaviours: tradeoff

learned behaviours: no tradeoff with stimulant, good performance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

adenosine functions (2)
+ A1 receptor (2)
+ A1 and A2 receptors (2)

A
  • inhibitory effect (glutamate antagonist)
  • dopamine antagonist
  • A1 receptor:
    • slowing metabolic function
    • postsynaptic depression of NMDA receptor important for learning
  • A1 and A2 receptors:
    • reducing heart rate
    • opening blood-brain barrier
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

caffeine behavioural effects

mood 2 + performance 4

A

mood elevation

    • placebo (dopaminergic release)
    • emotional physiological attribution

performance enhancement

    • enhanced in boring/simple tasks
    • disruptive or neutral in complex tasks
    • impaired decision-making in motor control
    • decrease in fatigue (but not getting better)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

caffeine absorption and elimination

A
  • time to peak/saturation is same across doses

- more experience -> longer effects (though reverse in cigarette smokers)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

caffeine tolerance and withdrawal + issues (3)

A

only physiological, not psychological

issues:

  • variability of absorption in studies
  • withdrawal or dehydration
  • small rates of systematic reported effects (11%)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

energy drinks + issues (3)

A

combination of xanthines + potentiatiors

issues:

  • highly variable xanthine content
  • natural caffeine doesn’t need to be listed
  • metabolites and precursors not measured
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Taurine (4)

A
  • similar to GABA: inhibitory in adults, excitatory in children
  • anxiolytic effects
  • shuts off acetylcholine retrograde learning mechanism
  • neuroprotectant (inhibits glutamate-induced excitotoxicity, antioxidant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Caffeine and Taurine together

A
  • synergistic effects: caffeine extremely potentiated

- aerobic heart pattern despite feeling chill

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

cocaine: administration (three ways)

A

chewing leaves

  • alleviates pain
  • alleviates altitude sickness

inhaling

  • paste mixed with kerosine: toxic
  • freebase: extracted paste, explosive
  • crack: freebase mixed with baking soda and water

injecting:
- hydrochloride: salt form of freebase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

cocaine: neuropharmacology (3)

A

reuptake inhibitor in mesolimbic pathway,
blocks transporter protein

  • reward: VTA
  • disordered thought/speech: PFC, nucleus accumbens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

issues in cocaine effects (3)

A

1) where does euphoria come from (dopamine, but not serotonin is affected, so wtf)
2) other transporter protein antagonists don’t induce euphoria
3) sensitization: larger euphoria and crashes in heavy users than non-heavy users

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

CART (cocaine and amphetamine regulated transcript)

midbrain and hypothalamus

A

midbrain: neuromodulator produced after psychostimulation
- if released with dopamine, inhibits action -> post-crash depression

hypothalamus: starvation
- responsible for decrease in eating behaviour(anorectic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

cocaine as antagonist

A

closes sodium channels -> no electric propagation -> anaesthesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

cocaine: long-term effects

A
  • anxiety/depression (downregulation in limbic system)
  • tremor (downregulation in midbrain)
  • suicide (motivation and disinhibition remain active)
  • delay discounting (evaluate outcomes differently based on when they’re obtained, especially for cocaine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cocaine: tolerance (rapid and physiological)

A

rapid tolerance:

  • coke-out (over 10-24h, same dose not same effect)
  • freeze (psychic numbing followed by exhilaration
  • let-down (depression after 1st dose due to coke-out)

physiological:

  • slow
  • heart-rate and blood-pressure effects
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

amphetamine: mechanisms

- molecular effects (3)

A
  • creates leaky vesicles
  • inhibits MAO (increase in dopamine)
  • inhibits reuptake of norepinephrine (9x), dopamine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

amphetamine:

  • Benzedrine
  • methylated amphetamine
  • ADHD treatment (dex vs levo)
A

Benzedrine:
- appetite suppressant, decongestant

methylated amphetamine:
- quicker passage across blood-brain barrier

ADHD treatment:

  • dex: higher binding affinity
  • levo: more potent but worse at binding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

amphetamine: tolerance (2)

A
  • tachyphylaxis

- study: positive effects on first meth days, negative effects on last meth day

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

amphetamine: dependence (2)

A

psychological (craving)
- anxiety/depression, sleep

crystal meth: physiological dependence, allostatic changes

22
Q

amphetamine psychosis (3)

A

1) chronic use:
- - paranoia, formication

2) delusions, hallucinations
- - dopamine release in limbic system

3) tweaking
- - irritability, violent behaviour

23
Q

ADHD: vigilant concentration

  • brain substrate
  • what happens in ADHD
A
  • reticular formation, norepinephrine
  • in ADHD: less norepinephrine, less perseverance
  • in ADHD: lack of sensitivity to rewards
24
Q

ADHD: cognitive awareness

  • brain substrate
  • what happens in ADHD
A
  • mesolimbic/mesocortical dopamine pathway hypoactive
  • any reward is motivating: ADHD kids respond to any reward but don’t follow through
  • inability to ignore stimuli
25
Q

Ritalin: neuropharmacology (3)

A
  • reuptake inhibitor for dopamine, norepinephrine
  • more potent inhibitor than cocaine
    • enters brain more slowly tho
    • thus, less abuse potential
26
Q

Ritalin

A
  • is an amphetamine
27
Q

(Dextro-) Amphetamines (Adderall) (3)

A
  • uniquely right-rotating
  • psychostimulants w/o vasoconstriction in body
  • psychoactive (decline in popularity)
28
Q

(Dextro-) Amphetamines (Adderall): neuropharmacology (3)

A

1) reverse dopamine transporter
2) create leaky dopamine vesicles
3) norepinephrine affected as well

29
Q

Ritalin, Adderall, Dex effects and abuse (3)

A
  • only moderate effects on cognition and WM
  • no effects on cognition or long-term memory
  • used as athletic enhancer (increased perseverance)
30
Q

ADHD medications: underprescription (3)

A
  • especially in ethnic minorities to escape stereotype
  • drug holidays
  • gateway drug belief (though actually more drug abuse in non-treated ADHD)
31
Q

cocaine vs ADHD medication (effects (2) and reinforcement (1))

A

effects

  • compared to Ritalin, shorter time to euphoria
  • compared to Amphetamine, less aversive acute and long-term effects

reinforcement
- combined reinforced schedule is best to get off cocaine

32
Q

permissive hypothesis

A

low serotonin causes low dopamine/norepinephrine

because if low serotonin, dopamine is compensated as precursor for serotonin -> less dopamine

33
Q

diathesis-stress model and MDD (3)

A
  • onset of MDD is correlated with stressful traumatic events
  • changes in schemas precede both onset and remission of depression, in response to stress
  • organic stress (e.g. low sunlight) can also induce depression-like symptoms
34
Q

first-generation antidepressants (2, what they do, problems)

A

1) MAO inhibitors
- inhibit MAO breaking down monoamines
- problem: MAO is used for breaking down many things
- - cheese reaction: if no MAO, no tyramine breakdown, stroke

2) tricyclics
- inhibit reuptake of serotonin, dopamine, norepinephrine
- problem: heart-rate irregular or elevated

35
Q

second-generation antidepressants (1)

A

SSRIs

  • inhibit serotonin reuptake
  • fewer cardiologic side effects than tricyclics
  • designed based on permissive hypothesis
36
Q

third-generation antidepressants (2)

A

SNRIs

- inhibit reuptake of serotonin and norepinephrine

37
Q

antidepressants, motivation, suicide

A

> take medication
motivation increases first, before mood
higher readiness to commit suicide (Black Box warning)

but: adolesents as likely to commit suicide on as off medication

38
Q

other drugs as antidepressants (3)

A

amphetamines:
- short-term euphoria, no long-term help

oxytocin:
- rewards interpersonal behaviour, in experimental phase

heterocyclics:

  • increase serotonin and norepinephrine in synapse
  • many problems though, only last resort
39
Q

problems with heterocyclics (4)

A
  • cardiovascular irregularities
  • downregulation of norepinephrine receptors (re-emergence of depressive symptoms)
  • high toxicity
  • other side effects (e.g. insomnia)
40
Q

antidepressants: discontinuation syndrome

+ reason given
+ withdrawal vs rebound
+ explanation

A

tendency to willingly stop taking the medication after 4 weeks, resulting in resurgence of symptoms

  • ‘brain shivers’ described after cessation
  • not withdrawal or tolerance-induced, but rebound
  • explanation:
    • feeling better, stop taking meds
    • takes long to have effect, think it ain’t working
41
Q

Glucocorticoid or BDNF theory of MDD

A

stress -> cortisol -> atrophy of hippocampus -> MDD

glucocorticoid:

  • released at end of HPA axis, induces cortisol release
  • HPA axis hyperactive
  • cortisol leads to changes in PFC, amygdala, hippocampus
  • treatment: antagonizing glucocorticoid receptors

BDNF:

  • facilitates neurogenesis of hippocampus
  • too little BDNF in MDD
  • treatment: serotonin agonists increasing BDNF production
42
Q

MDMA: absorption and elimination (solubility, MDA, CYP2D6)

A
  • highly lipid-soluble
  • metabolite MDA: psychoactive
    • longer high time
    • more potent
  • CYP2D6 enzyme needed to metabolize MDMA
  • SSRIs inhibit CYP2D6 -> dangerous to take MDMA when on SSRIs, toxicity
43
Q

MDMA: neuropharmacology (5 effects)

A

1) MAO-A inhibitor
2) competitive reuptake inhibitor (binds to reuptake transporter proteins)
3) leaky vesicles: expunge neurotransmitters out

4) reverse transport: expunge neurotransmitters out
- low doses: serotonin
- high doses: serotonin and dopamine

5) agonist at 5-HT receptors
- facilitates oxytocin release

44
Q

MDMA: acute effects (physiological + psychological)

A

physiological: sympathomimetic
- amphetamine-like
- sudden and extreme sympathomimetic response can lead to physiological problems, e.g. loss of consciousness

psychological: empathogenic
- increased empathy
- mild euphoria due to oxytocin
- sudden sympathomimetic resonse can lead to psychological problems, e.g. panic

45
Q

MDMA: negative effects (sub-acute, post-withdrawal, general)

A

sub-acute:

  • suicide Tuesday (depression/anxiety)
  • sleep disturbances
  • > both serotonin-related

post-withdrawal:
- substance-induced paranoid psychosis (low-level, false-yet-feasible beliefs of threat

general:

  • selective serotonergic neurotoxin
    • relapse of pre-existing mental illness (schizophrenia and bipolar)
    • lower seizure threshold
46
Q

MDMA: tolerance

A
  • mostly connection atrophy between serotonin-neurons, but neurons stay intact
  • serotonin downregulation and less serotonin release
  • weaker effects with more use
47
Q

MDMA: dependence

A
  • uncertain, not well documented
48
Q

MDMA: Brown et al. (2010)

A

> 3 groups: MDMA users, weed users, controls
match on many variables
test verbal working memory

  • > MDMA users poorer performance on all tasks
  • > long-term deficits in verbal memory
49
Q

MDMA: Hyseck et al. (2012)

reading emotions from eyes

A

> within: sober and high
reading emotions from eyes

  • > improved recognition of positive emotion
  • > decreased recognition of negative emotion
50
Q

MDMA: Kirkpatrick et al. (2014)

A

> sober, placebo, MDMA, oxytocin
morphed facial expressions test

MDMA:

  • > decreased ability to recognize angry and fearful faces
  • > no impact on happy faces

=> MDMA selectively impacts negative social perceptions

Drugs and Behavior 345A (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions