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Drugs and Behavior > Exam 3: Hallucinogens > Flashcards

Exam 3: Hallucinogens Flashcards

1
Q

3 broad categories of hallucinogens - what is in each (3)

A 
serotonin like (LSD, Peyote, Psilocybin, DMT)
belladonna alkaloids (acetylholine like, atropine, scopolamine)
dissociative anesthetics (PCP, ketamine, salvia)
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2
Q

substances that produce distortions of perception and of one’s sense of reality

A

hallucinogens

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3
Q

properties of psychadelic (mind expanding) drugs

A

alter sensory perceptions in brain
perceptual disturbances
changes in thought processing (used in religious ceremonies)

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4
Q

what schedule drug are hallucinogens?

A

schedule 1

- no accepted medical uses, high abuse liability

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5
Q

most hallucinogens are ___

what are effects

A

alkaloids

antibacterial, anitmitotic, anti-inflammatory, analgesic, local anesthetic, hypnotic, psychotropic, antitumor activity

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6
Q

LSD

A

schedule 1

synthetic drug derived from ergot

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7
Q

ergot

A

LSD
toxic parasitic rye fungus
alkaloids in ergot contract smooth muscles of veins and arteries (restricts blood flow), uterus (early labor), changes in BP
poisoning led to gangrene (loss of blood flow to extremities, they die off) and death in the middle ages
accidental small dose ingestion led to hallucinogenic effects

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8
Q

Project MKUltra

A

manipulated people’s mental status by giving LSD forcefully to force spys to reveal secrets

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9
Q

pharmacology of LSD (ADME and route of admin)

A

route of admin: oral - so potent it is delivered by stamps/blotter paper

A: 30-60 min post-ingestion from GI tract

D: BBB and NO depot binding

M: SLOW in the liver into 2-oxo-3-hydroxy-LSD

E: half like ~5 hrs

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10
Q

peyote

A

schedule 1
peyote cactus - peyote button cut off and dried cactus crown
active ingredient - mescaline (alkaloid)

psychoactive effects like LSD, BUT LSD is way more potent

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11
Q

pharmacokinetics of peyote(mescaline)

A

route of admin: oral-peyote buttons - chewed raw or cooked and eaten

A: rapid from GI tract, onset within 30min highest effects ~2hrs post ingestion, effects last up to 8hrs

D: poor lipid solubility, not easily through BBB - so need higher dose to get effects

M: ~50% broken in liver - main metabolite= 3,4,5-trimethoxyphenylacetic acid

E: excreted in urine in 24-48 hrs - even though need high dose it is out quick, 50% unchanged in urine

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12
Q

psilocybin

A

schedule 1
many species of magic mushrooms have alkaloids with hallucinogenic properties
cave paintings depicted as early as 3500 BC

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13
Q

Timothy Leary

A

psilocybin project

- teach people to self administer drugs to free syches without reliance on doctors

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14
Q

typical dose of psilocybin

A

1-2g o dried/powdered mushrooms

- way less than peyote (10-25 mg)

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15
Q

psilocybin pharmacokinetics

A

route of admin: dried mushrooms eaten raw, boiled in water for tea, cooked with other foods to mask biter taste

A: broken down into psilocin - active component, only 50% absorbed, psilocin detected in blood plasma 30 min after ingestion

D: BBB, psychoactive effects 10-40min after ingestion, last 2-6hrs

M: psilocybin converted to psilocin which is broken down by MAO

E: excreted unchanged or as psilocin-glucuronide in urine (65%), 20% excreted in bile and feces

psilocin detected in urine up to 7 days - in system for long time

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16
Q

glucuronide

A

psilocybin
substance produced by linking glucoronic acid to another substance via special chemical bond, makes water soluble

body does this when it comes across toxins

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17
Q

DMT

A

schedule 1
naturally occuring compound in body - biological function unknwon
low levels in brain
inc in response to stress
packaged and stores in neurotransmitter vesicles - serotonin

Ayahuasca

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18
Q

Ayahuasca

A 
DMT
tea
vine of the soul 
mix of 2 plants (one has DMT, other B-carbolines )
B-carbolines - inhibit MAO activity
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19
Q

what do you need to give DMT orally

A

MAO

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20
Q

what is DMT structurally similar to?

A

serotonin - share biosynthesis pathway
AADC converts tryptophan to tryptamine
tryptamine convets DMT to INMT

VMAT2 packages DMT into vesicles

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21
Q

pharmacokinetics of DMT

A

route of admin: smoked, snorted

A: DMT has no bioavailability taken orally - broken down by MAO, smoked or snorted produces short but very strong hallucinatory experiences

D: rapid to brain, active transport allows BBB, depot binding - small amount remains in brain for up to 7 days!!

M: metabolite= indole-3-acetic acid

E: rapid when taken WITHOUT MAO, excreted in urine in 24 hrs, 10% unchanged
if with MAO takes longer

22
Q

ayahuasca pharmacokinetics

A

tea taken orally
B-carbolines block MAO and DMT breakdown in liver so DMT reaches brain
hallucnogenic effects start 30-60min post ingestion
peak 1-2hrs dissipate 4hrs - longer to kick in

23
Q

effects of hallucinogens (8)

A 
hallucinations
altered perceptions
profound effects on mood
altered thinking processes
altered physiological processes
altered state of consciousness
feeling of being separated from body 
psychosis
24
Q

psychadelic effects time frame

A

begin 30-90min after ingestion
LSD trip can last 6-12 hrs
smoked DMT effects felt within seconds, peak over a few minutes, gone in an hour

25
Q

flashbacks

A

re-experiencing hallucinations after chronic use, years later eventhough drug use stopped
unc;ear why

26
Q

what determines if you will have a good or bad trip

A

dose, personality, previous drug experiences, context

27
Q

4 phases of LSD trip

A

onset: 30min-hr after LSD
1st feel behavioral effects

plateau: 2 hrs in , time slows- perception it has been a long time
peak: 3 hrs in , synesthesia , most hallucinations

come-down: 5-6 hrs in

28
Q

synesthesia

A

crossing of sensory modalities

ex: feeling sounds or hearing colors

29
Q

smoking DMT effects over time

A

lungs burn, cough
loud sound in ears until feel yourself blow up and enter universe
break into another universe - heart beats faster
you have left body
visions fade out
euphora lats 30min ater visual trip

30
Q

physiological effects of hallucinogens

A 
sympathetic nervous system
- pupil dilation
inc HR BP T
restlessness
dizziness, vomiting, nausea - peyote and ahowasa
31
Q

LSD, DMT, and psilocin are chemically similar to…

A

serotonin

32
Q

mescaline is structurally similar to..

A

NE and amphetamine (metabolite p-hydroxymethamphetamine had hallucinogenic effects)

33
Q

LSD binds with high affinity to at least ____ different serotonergic receptor subtypes

A

8

34
Q

LSD, mescaline, DMT, and psilocin bind to what type of receptors and are what agonists

A

serotonin receptors

5-HT2A receptor agonists

35
Q

hallucinogenic properties require the activation of what receptor subtype?
and… this alters levels of what neurotransmitter in cerebral cortex?

A

5-HT2A receptors

glutamate levels altered

36
Q

why is LSD so potent?

why do its effects last so long?

A

LSD binding to 5-HT2A forms lid that locks LSD in place temporarily trapping it
lacks ability to unbind
sustained activation

37
Q

where are 5HT2A receptors found

A

raphe, PFC, locus coeruleus

38
Q

activation of 5HT2A receptors increases the release of what into the cerebral cortex to turn on PFC

A

glutamate

39
Q

what do EEG studies show about hallucinogens

A

they disrupt the normal rhythmic oscillations in the cerebral cortex
- added extra stimuli for them to attend to that they would normally ignore

40
Q

effect of hallucinogen on visual cortex

A

alters visual processes, including modal object completion

activation of occipital lobe

41
Q

effect of hallucinogens on temporomedial cortex

A

inc activity - complex visual processing , integration area

some auditory hallucinations

42
Q

effects of hallucinogens on cerebral cortex

A

inc sensory signals to PFC

43
Q

effect of hallucinogens on locus coeruleus

A

dec spontaneous activity, sends normal suppressed sensory info to cerebral cortex
sleep states, dream like states

44
Q

effects of hallucinogens on PFC

A

inc activity of PFC

central sensory integration area of cerebral cortex

45
Q

serotonin receptor binding causing hallucinations: thalamus

A

involved in sensory routing and sleep (reticular patwhay - arousal) - hallucinations like dreams
activate your dreams while you are awake

46
Q

sertonin receptor binding causing hallucinations in limbic pathway

A

emotional investment/context of meaning of hallucination vs dream
when ppl scared bc of a bad trip - see something scary in their environment like monsters chasing them
entorhinal cmpus and hippocampus for context

47
Q

do hallucinogens produce depence and withdrawal symptoms

A

no

48
Q

what hallucinogens produce rapid tolerance to repeated use through down regulation of 5HT2A receptors

A

most hallucinogens EXCEPT DMT

49
Q

push to re-evaluate therapeutic uses for what 2 hallucinogens

A

psilocybin and LSD

50
Q

why would hallucinogens improve mental health

A

when consume they have experience when they come off of it they get an afterglow period!!!

51
Q

afterglow period

A

gives clarity, reduces negative affect (anxiety, fear, depression) in state of well being and calmness
it persists for days - longer time
used to treat long term chronic issues

Drugs and Behavior (27 decks)

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