Chapter 15: Hallucinogens Flashcards

1
Q

LSD is a ____ agonist, and ketamine is a ____ antagonist

A

LSD is a 5-HT2a agonist, and ketamine is an NMDA antagonist

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2
Q

LSD was derived from ____ fungus

A

ergot

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3
Q

who discovered LSD

A

Albert Hoffman

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4
Q

main method of administration of LSD

A

oral injestion

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5
Q

4 main categories of hallucogenic effects

A

1) phantasticants
2) psychodelics
3) entactogens
4) psychomimetics

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6
Q

characteristics of a phantasticant

A

spiritual enlightenment

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7
Q

psychodelic characteristics

A

manipulation of senses, more intense colors

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8
Q

T/F: psychodelic drugs cause hallucinations

A

false, everything you see is real, but just more intense. things may be wavy with brighter colors

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9
Q

characteristics of entactogens

A

feelings of insight

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10
Q

characteristics of psychomimetics

A

beliefs or seeing things that aren’t there, hallucinations

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11
Q

where does LSD metabolism take place

A

mostly in the liver

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12
Q

T/F: LSD is a selective serotonin receptor agonist

A

true. it has a high affinity for 5-HT2a

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13
Q

a common mechanism of action of all hallucinogenic drugs

A

they almost all increase activity in the prefrontal cortex, and have common downstream effects

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14
Q

Which brain structures are affected, causing more vivid experiences while on LSD?

A

LSD increases the sensitivity of the thalamus, which is the brain region responsible for relaying external stimuli to the brain

3 primary brain regions (from book)

1) locus coeruleus (limbic system)
2) the cortex
3) raphé nuclei; usually helps filter incoming stimulus. increasing levels of serotonin over activate the raphé and it filters less stimuli

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15
Q

T/F: LSD causes huge stimulation in the mesolimbic dopamine system

A

false, it gives less stimulation to the mesolimbic dopamine system than caffeine

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16
Q

list some monoamine-like hallucinogens. some dissociative anaesthetcis?

A

monoamine like: LSD, magic mushrooms, mescaline, MDMA

dissociative anaesthetics: PCP, ketamine

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17
Q

in the cortex, how does LSD and hallucinogens increase activity?

A

they increase the duration of glutaminergic excitatory action potentials by acting on the excitatory 5-HT2a receptors, turning on the glutamate neurons

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18
Q

hypnogogic states in LSD-like drugs

A

Hypnogogic states: a state of imagination just before you fall asleep

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19
Q

T/F: people on LSD have increased susceptibility to hypnosis

A

true

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20
Q

T/F: time speeds up on LSD

A

false, most people report slowing down while on LSD

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21
Q

T/F: people have increased susceptibility to hypnoses while on LSD

A

true

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22
Q

entactogenic symptoms while on LSD-like drugs

A

provideing insight into one’s past and one’s own mind. serious introspection going on.

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23
Q

LSD’s effect on memory

A

there is a deficit in short-term and working memory

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24
Q

How can LSD like drugs be used as an antidepressant?

A

LSD is a 5-HT2a agonist and increases amount of serotonin in the brain. increased serotonin incresaes BDNF stimulation, contributing to synaptic remodeling

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25
Q

Why can you not overdose on LSD?

A

because it is a partial 5-HT2a agonist and will not cause serotonin syndrome

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26
Q

comment on the tolerance effects of LSD

A

if you take it daily, some tolerance will occur, but sensitization will come back within a week. there is cross tolerance to other mono-amine like drugs like magic mushrooms and mescaline. Tolerance is due to downregulation of serotonin 5-HT2a receptors

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27
Q

T/F: there is cross tolerance from LSD to cannabis

A

false

28
Q

withdrawal effects of LSD

A

none

29
Q

Is LSD discriminable from saline

A

heck yes

30
Q

what other drugs do LSD generalize to?

A

it generalizes to some other monoamine hallucinogens but not dissociative anaesthetics

31
Q

are LSD-like drugs readily administered

A

no, monkeys will even move away from the site of administration. Humans usually only administer it if they’re curious

32
Q

which monoamine would monkeys readily administer? why?

A

they would administer MDMA because in addition to the hallucinogenic effect, it acts as a psychomotor stimulant like methamphetamine and activates the reward system. the monkeys begin to associate hallucinations with reward and will thus take MDMA

33
Q

acute psychotic reaction /psychedelic crises

A

a “bad trip,” causing terror and anxiety

34
Q

trailing phenomena

A

seeing after images as something moves.

35
Q

what increases the “danger” level of LSD?

A

if you take MAOI’s with it. In addition to LSD stimulating serotonin release, there is nothing else breaking down the chatecholamines/monamines in the synapse.

36
Q

combining MAOIS and LSD can lead to ____ toxicity

A

serotonin toxicity; the death of terminals due to too much monoamine transmission

37
Q

synthetic MDMA is similar to natural ____, (from a cactus), but is way more potent

A

MDMA is similar to mescaline but is way more potent

38
Q

how is MDMA synthesized?

A

by modifying amphetamine. it thus produces rewarding and hallucinogenic effects

39
Q

mechanism of MDMA, how is it different than LSD?

A

MDMA stops the SERT transporters in the presynaptic cell from working, and so serotonin cannot be taken back up into the cell. different than LSD because LSD acts on 5-HT2a receptors POST synaptically like most neurotransmitters.

40
Q

in addition to disabling the serotonin transporters, how else does MDMA achieve its effects?

A

it also has effects on dopamine and affects the release of oxytocin.

41
Q

why is MDMA less safe than LSD

A

because it has no safety net. it is a full agonist of 5-HT2a unlike LSD, which is impossible to overdose on.

42
Q

why was MDMA given during therapy?

A

because it increases therapeutic alliance, people agreed to work more with the therapist and it enhances communication

43
Q

what does MDMA generalize to?

A

other serotonin agonists (5HT1A)

44
Q

T/F: MDMA generalizes to cocaine

A

false

45
Q

how does MDMA effect body temp? Why is this risky?

A

it increases body temp. people often try to drink water to cool down but they end up swelling their brain and causing epileptic-like seizures

46
Q

main cause of death from MDMA

A

hyperthermia (over heating) and hypernatremia ( loss of electrolytes)

47
Q

how do dissociative anaesthetics work

A

they separate people from sensory experience

48
Q

disscoiative anaesthetics like ketamine are ____ antagonists

A

NMDA antagonists

49
Q

is PCP more potent than ketamine

A

no, ketamine is more potent than PCP, has stronger effects but lasts a shorter amount of time

50
Q

how does PCP and ketamine produce rewarding effects?

A

NMDA antagonist inhibits the GABA interneuron, resulting in increased Dopamine in the mesolimbic dopamine reward system

51
Q

in what way does PCP and ketamine separate people from sensory experience?

A

by removing emotional value. people become less bothered by pain.

52
Q

Why does PCP and ketamine result in memory problems?

A

because NMDA blockers affect the hippocampus from generating memories, like alcohol

53
Q

are dissociative anaesthetics lipid soluble?

A

yes, they are normally injected

54
Q

how does PCP and ketamine contribute to hallucinogen affects?

A

it increases cortical activity by blocking the NMDA receptor on GABA neurons in the brain. with no GABA inhibiting the cortex, cortical activity rises.

55
Q

relationship of ketamine and BNDF

A

it actually stimulates BDNF

56
Q

generalizability of dissociative drugs.

A

animals who can discriminate PCP and ketamine will not generalize them to any other class of drugs, there is some generalization to LSD though, most likely due to commonalities with the 5-HT2a receptors.

57
Q

withdrawal affects of PCP

A

teeth grinding, anxiety and confusion

58
Q

the one drug that generalizes to PCP and ketamine

A

dextromethorphan. NMDA antagonist

59
Q

where in the brain is seen to have a reduction in volume upon PCP and ketamine use

A

there is decreased volume of the frontal gyrus

60
Q

roboing

A

taking a bunch of cough syrup that contains dextromethorphan

61
Q

Salvia is a _____ agonist

A

kappa opioid receptor agonist

62
Q

how does salvia counteract kappa agonism resulting in decrease DA?

A

salvai is also a partial D2 agonist, allowing for hallucinations with no kappa induced DA decrease

63
Q

What neurotransmitters do GHB modulate?

A

dopamine and GABA by binding to GHB receptors and GABAb receptors

64
Q

where are GHB receptors primarily located?

A

in the cortex and hippocampus, resulting in decrease memory function

65
Q

what disorder is GHB good at treating?

A

narcolepsy

66
Q

T/F: reinforcing effects of MDMA is similar to psychomotor stimulants

A

false. psychomotor stimulants like amphetamine increase dopamine transmission in the mesolimbic system, but MDMA seems to mediated by its relationship with 5-HT2a receptors.