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Drugs and Behavior 345A > midterm #3 > Flashcards

midterm #3 Flashcards

1
Q

hallucinogens:

  • psychedelic
  • entheogenic
  • psychotomimetic
  • psycholytic
A

psychedelic: manifesting the mind, mind-expanding
entheogenic: religious or spiritual
psychotomimetic: appearance of psychosis
psycholytic: mind-dissolving

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2
Q

hallucinogens operationalization

A

“chemical inducing perceptions of something that doesn’t exist”

problem:

  • more distort reality, therefore illusionogenic
  • many things can induce hallucinations at toxic levels
  • hard to keep apart from delirium related to toxicity
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3
Q

psychedelics: reducing valve
dissociatives: numbing, depersonalisation, derealisation
deliriants: confusion

A

psychedelics:
- reducing valve: feeling that the brain’s filter has been removed

dissociatives:

  • numbing: analgesia, amnesia, anaesthesia
  • depersonalisation: dream-like or unreal perception
  • derealisation: detached or removed from body

deliriants:
- confusion, inability to control behaviour

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4
Q

hallucinogen structural similarities:

  • serotonin
  • norepinephrine
  • no similarity
A

serotonin: LSD, psilocybin, DMT
norepinephrine: ecstacy, mescaline
no similarity with anything: PCP, Ketamine, Salvia

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5
Q

general hallucinogen process (2 stages)

A

stage 1: visual images

  • geometric patterns
  • closed-eye, then open-eye

stage 2: meaningful images

  • people/animals/places
  • can change rapidly
  • recognized as not being real
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6
Q

LSD: 4 general points

A
  • derived from ergoline in ergot fungus
  • highly volatile (water-soluble, oxidizes, photosensitive)
  • highly potent (1 dose = 50-150µg)
  • sympathomimetic
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7
Q

LSD process:

  • onset
  • plateau (4 effects)
  • peak (3 effects)
A

onset

  • 30-60min
  • release of tension

plateau

  • 30min-2h)
  • closed-eye visuals
  • synaesthesia
  • multilevel reality perception (insula)
  • distorted visual input (locus coeruleus/visual cortex)

peak

  • 3-5h
  • emotion/panic swings
  • timelessness
  • ego disintegration (PFC, glutamate)
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8
Q

LSD neuropharmacology

  • visual cortex
  • locus coeruleus
  • PFC
A

=> agonism

visual cortex:

  • 5-HT1A, 5-HT2A receptors
  • decreased activity

locus coeruleus:

  • metabotropic 5-HT2A receptors on glutamatergic and GABAergic neurons
  • lower threshold for incoming sensory signals
  • decrease in noise

PFC:

  • induced glutamate release
  • PFC tries to frantically interpret perceptions
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9
Q

LSD: tolerance

A
  • acute tachyphylaxis
  • 3-7 days to subside
  • cross-tolerance to other tryptamines (psilocybin and DMT)
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10
Q

LSD: toxicity

A
  • myadrasis: chronic pupil dilation
  • serotonin syndrome
  • hallucinogen persisting perceptopn disorder (HPPD)
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11
Q

serotonin syndrome

A

accumulation of excess serotonin in CNS

  • symptoms:
    1) cognitive: hypomania, confusion, hallucinations
    2) autonomic: sweating, hypothermia, vasocontrition, tachycardia
    3) somatic: tremor, twitchiness
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12
Q

psilocybin: qualitative differences in dosage

A

low: social, warm, down-to-earth feelings
high: resemble LSD, but more prone to bad trips

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13
Q

psilocybin: neuropharmacology
- PFC
- basal ganglia

A

=> partial agonism

PFC:

  • 5-HT2A
  • distort time perception, timing, feel for rhythm
  • slowing down
  • inability to coordinate with tempo <2-2.5s

basal ganglia:

  • dopamine
  • problem: no affinity for D2 receptor
  • may be involved in timed performance and movement
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14
Q

psilocybin: tolerance

A
  • acute tolerance
  • 4-7 days to subside
  • cross-tolerance to LSD and phenethylamines
  • potentiation when used with MAO-inhibitors
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15
Q

psilocybin: therapeutic uses

A

reduction of 5-TH2A receptors

  • alleviation of OCD symptoms for 2 months
  • anxiolytic
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16
Q

psilocybin: Good Friday Experiment

A
  • increase in spiritual meaning
  • positive changes in attitude/behaviour
  • effects for weeks/months after treatment
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17
Q

ibotenic acid: 4 points (origin, functionally, structurally, metabolite)

A
  • from Muscaria mushrooms
  • functionally similar to glutamate (non-selective glutamate agonist)
  • structurally similar to acetylcholine
  • metabolite muscimol also psychoactive
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18
Q

ibotenic acid:

  • danger
  • how to prevent
A
  • excitotoxicity causes subjective effects and brain damage

- dextromorphan (cough syrup) can protect from excitotoxicity by blocking receptors

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19
Q

PCP:

  • embalming fluid
  • Angel Dust
  • killer joints
A

embalming fluid: yellowish oil to dip cigarettes or joints in

Angel Dust: crystals ground and sprinkled on a mix of spices, then smoked

killer joints: mix with weed

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20
Q

PCP and Ketamine: neuropharmacology

  • low dose
  • high dose
  • any dose
A

low dose:

  • serotonin and dopamine
  • reuptake inhibition
  • partial agonist

high dose:

  • acetylcholine
  • antagonism (muscle contractions, memory deficits, arousal, analgesia)

any dose:

  • glutamate NMDA antagonist
  • disrupts LTP
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21
Q

PCP and Ketamine: dose-dependent effects

  • low dose
  • moderate dose
  • high dose
A

low dose:
- drunk-like, numbing, anaesthetic

moderate dose:

  • disconnect from surroundings
  • body dissociation

high dose:

  • sympathomimetic
  • hallucinations
  • K-hole
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22
Q

PCP and Ketamine:

  • high-dose negative consequences
  • long-term use negative effects
A
  • lingering schizophrenic-like symptoms for up to 2 months
  • supports glutamate hypothesis of schizophrenia
  • chronic glutamate antagonism leads to MDD-like symptoms and deficits in memory, speech, logic
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23
Q

PCP and Ketamine: 2 weird effects

A
  • superhuman strength and invulnerability feeling (due to analgesia)
  • megalomania: delusional fantasies of omnipotence and god-like power
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24
Q

PCP and Ketamine: tolerance

A
  • accrued tolerance (can be prevented by separating administrations by days)
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25
Q

PCP and Ketamine: dependence

A
  • physical: in PCP dopaminergic centres affected, Ketamine no physical dependence
  • psychological: craving related to euphoria
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26
Q

Ketamine Psychedelic Therapy: Morrough (2012) results

+ glucocorticoid theory explanation

A

treatment-resistant MDD: one dose alleviation of symptoms within hours, lasting more than a week

glucocorticoid theory: glutamate NMDA inhibition allows for glutamate to bind elsewhere and facilitate BDNF

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27
Q

structure-activity relationship

A

relationship between a chemical’s structure and its biological activity

28
Q

debate: DMT endemic to human body (just look at these)

A
  • present in other mammals’ pineal glands
  • enzyme found in human body but not brain
  • DMT analogue synthesis in human cancer cells in lab setting
  • facilitation of immune responses on endemic receptors after taking DMT
29
Q

DMT: neuropharmacology

  • 3 stages
    • what neurotransmitter
    • where
    • most important characteristics
A

=> agonist (SNDRA)

dopamine: o1 related to sensations
(1)
- insula
- auditory hallucinations

(2)

  • amygdala
  • waiting room, animated suspension
serotonin: 5-HT2A, 5-HT2C
(3)
- PFC
- DMT Hyperspace
- Machine elves
30
Q

DMT: tolerance

A
  • debate whether none or acute
  • perhaps short time activating receptors makes it skip the whole tolerance thing
  • cross tolerance: from LSD to DMT, but not from DMT to LSD
31
Q

DMT: dependence

A
  • no physical dependence
  • psychological dependene debated
  • religious connotation may protect from dependence
32
Q

DMT: insight-oriented psychotherapy

  • for PTSD, anxiety, phobia
  • for depression, addiction
A

for PTSD, anxiety, phobia:
- rationalization, remove emotional component

for depression, addiction:
- therapeutic insight about fears, beliefs, desires

33
Q

DMT therapeutic potential (3)

A
  • elicits traumatic memories
  • offers multiplicity of perspectives
  • promotes LTP for connections underlying new perspectives
34
Q

phytocannabinoids: 4 general points

A
  • metabolites of THC are active
  • metabolites exert unique effects interacting with THC
  • analogues exert unique effects e.g. 11-hydroxy-THC
  • highly lipid-soluble
35
Q

synthetic cannabinoid alternatives

A
  • K2, Spice
  • stem from research on receptors
  • aminoalkylindoles -> target serotonin system
  • stimulant and hallucinogenic properties b/c contamination with other chemicals
36
Q

cannabis potency: hash vs marijuana

+ 3 problems

A

hash more potent than marijuana

problems:

1) dosages vary and effects are dose-dependent (2-6x more THC in hash than MJ)
2) modern strains much higher concentration
3) skewed comparability of research from today and earlier

37
Q

cannabis: smoke
- % absorbed
- contact high

A

smoking:
- 50% of THc is released into smoke
- lungs absorb about 20% of that

contact high:
- no hard evidence, only if strong hotbox

38
Q

cannabis: ingestion
- % absorbed
- how long stays

A
  • first.pass metabolism deactivates 50% of THC
  • 4-5 days of use lead to ca. 7 days of long-term pharmacological action
  • metabolites still psychoactive, but less than in smoking
39
Q

cannabis: neuropharmacology

A

=> partial agonism

metabotropic receptors CB1 and CB2

  • CB1: motor inhibition, ood, memory, appetite, pain
    • reduces presynaptic firing rate
  • CB2: immuno-facilitative (glial cells)
40
Q

THC: motor activity/coordination and RT effects (low and high dose)

A

low dose: increase motor activity, decrease coordination
high dose: decrease motor activity, increase RT

compensate for disrupted vigilance by driving more slowly though

41
Q

THC: amotivational syndrome

A

-> persistent lack of motivation to engage in productive activities

  • no evidence for reward-based strategies (when tasks provide rewards)
  • actually: cannabis makes effortful tasks seem less effortful
42
Q

THC: short-term memory and attention impairment (low and high dose)

A

low dose: memory deficits, no attention impairment

high dose: memory, attention, reasoning impairment

43
Q

cannabis: developmental persistence

A
  • for every 5 years of marijuana use, 1-word decrease in verbal memory of a 15-word list
  • no other impairment in cognitive functions

=> weed associated with worse verbal memory

44
Q

cannabis: decelerated time - associations (4)

A
  • associated with stoned phase
  • decreased blood flow to cerebellum
  • temporal disintegration: no continuous temporal processing
  • flight of ideas: spontaneous random thoughts, decreased cognitive threshold
45
Q

THC: executive function impairment

A
  • updating WM / shift / inhibiiton

- chronic users: impairment while abstinent

46
Q

cannabis: gateway drug

A
  • support for process, but not outcome
  • problems:
    • not all users progress to next drug (only 10-20%)
    • users still use early drugs
47
Q

cannabis: gateway drug vs correlated vulnerabilities

A
  • drug use progression is due to user’s characteristics, not due to drug properties
  • individual propensity for drug use defines process
48
Q

cannabis: long-term verbal fluency and divided attention

A
  • compared to non-users, differences in
    • verbal fluency
    • divided attention (persevering on previous rules)
49
Q

cannabis: intellectual impairment

A
  • intellectual impairment of heavy users reversed with abstinence
50
Q

cannabis onset <17

A
  • severe verbal and IQ deficits

- 40% higher chance for schizophrenia, GAD, depression

51
Q

cannabis tolerance and withdrawal

A
  • downregulation with prolonged use

- withdrawals (irritability, insomnia, hostility) dissipate after 6 weeks

52
Q

Cannanbis Hyperemesis Syndrome

+ supportive features

A

nausea, vomiting, colicky abdominal pain as result of weekly cannabis use following a history of cannabis use for years
(-> physiological, outcome, no allergy)

supportive features:

  • taking compulsive hot showers
  • colicky abdominal pain (possibly due to toxic buildup)
53
Q

THC: toxicity

A
  • in plant, low toxicity, no ODs reported

- dronabinol, toxic effects (e.g. postural hypotension, slurred speech); pure THC

54
Q

THC: drug discrimination (vs placebo, vs other drugs)

A

THC vs placebo:
- 100% accuracy

THC vs other drugs:

  • low dose: 100% accuracy
  • high dose: 85% accuracy

=> THC has unique subjective effects

55
Q

cannabis: different cannabinoids have different effects

A
  • THC users: higher incidence of hallucinations/delusions
  • no difference non-users and THC+CBD users
  • CBD users: anxiety reducing
56
Q

heroin, morphine: intake and effects (3)

A

oral: mood alleviation, cough suppression
inhalation: euphoria
intravenous: euphoria, pain relief

57
Q

heroin morphine injection: 3 stages

A

stage 1:

  • 0-2min
  • rush
  • tingling lower abdominal feeling, orgasm

stage 2:

  • 2-3h
  • on the nod: tranquil drowsiness

stage 3:

  • 4+h
  • withdrawal
58
Q

fentanyl (4)

A
  • designed
  • 100x more potent than morphine
  • intake: oral, transdermal, insufflation, but: fast absorption has high potential for respiratory depression
  • less nausea and itching than morphine
59
Q

desomorphine

A
  • synthesized from codeine
  • 8x more potent than morphine
  • increased respiratory depression and cardiac arrest
  • high toxicity from impurity and contamination
60
Q

opioids: neuropharmacology

A

=> agonism

1) cleavage enzyme: cuts free-floating inactive peptides into active metabolites
2) G-protein metabotropic action: returns neurons to resting potential sooner

61
Q

opioids: agonism pure, partial, mixed

A

pure: pain relief
partial: pain relief w/o respiratory effects
mixed (agonist-antagonist): treating opioid addiction - binds to receptors without activating them, but blocks other chemicals from binding

62
Q

opioids:

  • agonistic mechanism
  • inhibitory mechanism
A

agonistic mechanism:

  • GABA receptor antagonist
  • VTA: stops inhibition of dopamine release
  • NA: activates µ-opioid receptors that inhibit GABA neurons
  • > dopamine release in VTA

inhibitory mechanism:

  • nociception
  • interferes with pain signalling from periphery to spinal cord and spinal cord to thalamus
  • > blunting of pain
63
Q

opioids: tolerance

A
  • dose-dependent
  • accrued and relational
  • tolerance selective to analgesia, euphoria, respiratory depression
64
Q

opioids: withdrawal

A
  • 5-10 days
  • 90% relapse after withdrawal related with environment
  • craving instensifies at 1-3 days
  • flu-like symptoms
65
Q

opioids: detoxification

A

rapid (10 days):

  • naloxone
  • inverse agonist, binds and induces opposite response
  • increased withdrawal symptoms, decreased duration

short- (30 days) or long-term (180 days):

  • methadone
  • prevents withdrawal, weak/no euphoria
  • long-lasting effects
66
Q

DMT: The Hoasca Project results

A
  • ayahuasca-sect adolescents 7x lower incidence of anxiety, body dysmorphism, attention problems
  • > religious context has protective effect

Drugs and Behavior 345A (3 decks)

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