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Behavioral Pharmacology > Chapter 15: Hallucinogens, PCP, and Ketamine > Flashcards

Chapter 15: Hallucinogens, PCP, and Ketamine Flashcards

1
Q

Altered States of Consciousness (ASC) rating scale

A

Psychometric scale developed to quantify the subjective effects of hallucinogenic agents.

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2
Q

dimethyltryptamine (DMT)

A

Hallucinogenic drug found in several South American plants.

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3
Q

dissociative anesthesia

A

An unusual type of anesthetic state characterized by environmental detachment. It is produced by certain noncompetitive NMDA receptor antagonists such as ketamine and PCP.

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4
Q

flashback

A

Reexperience of the perceptual drug effects, specifically those of a hallucinogen, following termination of drug use; when flashbacks occur a long time after prior drug use and are intense the individual is experiencing hallucinogen persisting perception disorder (HPPD)–not common

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5
Q

Hallucinogen Rating Scale

A

Psychometric scale developed to quantify the subjective effects of hallucinogenic agents.

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6
Q

indoleamines

A

Indole derivatives containing an amine group. They include serotonin and the hallucinogens LSD, psilocybin, psilocin, DMT, and 5-MeO-DMT.

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7
Q

ketamine

A

Drug that binds to the PCP site and acts as a noncompetitive antagonist of the NMDA receptor. It is a dissociative anesthetic used in both human and veterinary medicine, and it is also used recreationally.

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8
Q

lysergic acid diethylamide (LSD)

A

Hallucinogenic drug that is synthesized from lysergic acid and based on alkaloids found in ergot fungus. It is thought to produce its effects mainly by stimulating 5-HT2A receptors in the brain.

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9
Q

mescal button

A

Crown of the peyote cactus, Lophophora williamsii, which can be dried and ingested to obtain the hallucinogenic drug mescaline; chewed or cooked raw or extracted as a pure powder.

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10
Q

mescaline

A

Hallucinogenic drug produced by several cacti species, especially that of the peyote cactus, Lophophora williamsii.

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11
Q

5-methoxy-dimethyltryptamine (5-MeO-DMT)

A

Hallucinogenic drug found in certain South American plants. Its street name is “foxy” or “foxy methoxy.”

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12
Q

para-chlorophenylalanine (PCPA)

A

Drug that irreversibly inhibits tryptophan hydroxylase, blocking 5-HT synthesis.

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13
Q

peyote button

A

Species of cactus, Lophophora williamsii, that produces mescaline.

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14
Q

phencyclidine (PCP)

A

Drug that binds to the PCP site and acts as a noncompetitive antagonist of the NMDA receptor. It is a dissociative anesthetic that was once used medicinally but is now only taken recreationally.

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15
Q

phenethylamine

A

Class of drugs that includes mescaline as well as NE- and amphetamine-related substances.

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16
Q

psilocin

A

Metabolite of psilocybin. Psilocin is the actual psychoactive agent.

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17
Q

psilocybin

A

Hallucinogenic drug found in several mushroom species; take 1-5g for effect.

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18
Q

psychedelic

A

Substance that alters perceptions, state of mind or awareness; “mind-opening”

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19
Q

psychedelic therapy

A

Therapeutic method that involved giving patients a single high dose of LSD to help them understand their problems by reaching a drug-induced spiritual state.

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20
Q

psychotomimetic

A

Substance that mimics psychosis in a subject, such as by inducing hallucinations or delusions.

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21
Q

salvinorin A

A

Active compound in the hallucinogenic plant Salvia divinorum; acts as a κ-opioid receptor agonist.

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22
Q

synesthesia

A

Mixing of sensations such that one kind of sensory stimulus creates a different kind of sensation, such as a color producing the sensation of sound.

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23
Q

hallucinogens

A

substances whose primary effect is to cause perceptual and cognitive distortions without producing a state of toxic delerium

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24
Q

what happens to psilocybin when ingested?

A

it is enzymatically converted to psilocin, which is the actual psychoactive component

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25
Q

ayahuasca

A

hallucinogenic brew from stalks and leaves containing DMT and vines containing several types of alkaloids called beta-carbolines, which are known to inhibit the enzyme MAO

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26
Q

synthetic DMT analogs

A

AMT and Foxy

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27
Q

how is DMT and 5-MeO-DMT taken?

A

it is found in a number of plans and is typically turned into a drink

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28
Q

is LSD natural?

A

no it is synthetic

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29
Q

analeptics

A

circulatory and respiratory stimulants

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30
Q

psycholytic therapy

A

based on the concept of drug-induced psycholysis–meaning psychic loosening or opening. Involved giving LSD in low but gradually increasing doses to promote the release of repressed memories and to enhance communication.

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31
Q

administration of LSD

A

orally

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32
Q

administration of salvia

A

chew fresh salvia leaves, smoke dried and crushed leaves, consume concentrated salvinorin A-containing extract either sublingually or through smoking; few if any psychoactive effects are produced by swallowing salvia but is rapidly and easily absorbed into the lungs if smoked

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33
Q

does salvia exert psychoactive effects if you eat it?

A

few if any psychoactive effects are produced by swallowing salvia; it is inactivated in the GI tract

34
Q

subjective effects of saliva

A
  • becoming objects
  • visions of various two-dimensional surfaces, films, and membranes
  • revisiting places from the past, especially childhood
  • loss of the body and/or identity
  • various sensations of motion or being pulled or twisted by forces of some kind
  • overlapping realities; the perception that one is in several locations at once
35
Q

Potency of hallucinogenic drugs

A

from most to least

  • LSD (oral)
  • salvia (smoking)
  • psilocybin (oral)
  • DMT (smoking)
  • mescaline (oral)
36
Q

duration of drug effects

A

effects generally begin within 30 to 90 minutes following ingestion. LSD and mescaline effects last between 6-12 hours or longer, with psilocybin-containing mushroom trips being a bit shorter. DMT and salvia’s effects are felt within seconds, reach a peak over minutes and are done within an hour

37
Q

what can impact drug effect’s duration

A

the dose and when the user last ate

38
Q

trip phases

A
  1. onset
  2. platea
  3. peak
  4. come-down
39
Q

trip onset

A

occurs 30-60 minutes after taking LSD; visual effects occur, colors intensify and appearance of geometric patters or strange objects that can be seen when eyes are closed

40
Q

trip plateau

A

after onset and lasts ~2 hours; sense that time begins to slow and the visual effects become more intense

41
Q

trip peak

A

begins about after three hours and lasts for 2-3 hours; feeling like in another world where time is suspended, may experience synesthesia, continuous stream of bizarre, distorted images

42
Q

trip come-down

A

lasts ~2 hours; most drug effects are gone after the come down but user may not feel normal until the next day

43
Q

what are psychological changes that are associated with taking hallucinogenic drugs?

A

depersonalization, emotional shifts to euphoric, anxious, or fearful states, disruption of logical thought

44
Q

physiological effects of LSD

A

activation of the sympathetic nervous system–pupil dilation, small increases in heart rate, blood pressure and body temperature; can also cause dizziness, nausea, vomiting

45
Q

what are the two types of structures of hallucinogenic drugs?

A

serotonin-like (idoleamine) and catecholamine-like (phenethylamine)

46
Q

serotonin-like (idoleamine) drugs

A

LSD, psilocybin, psilocin, DMT, 5-MeO-DMT, synthetic tryptamines

47
Q

catecholamine-like (phenethylamine) drugs

A

mescaline

48
Q

catecholamine-like (phenethylamine) structure

A

structure is similar to NE and amphetamine

49
Q

chemical structure of salvinorin A

A

neoclerodane diterpene

50
Q

what does LSD bind to with high affinity?

A

at least 8 different serotonin receptors

51
Q

Common sites of interaction for both catecholamine-like (phenethylamine) and serotonin-like (idoleamine) drugs?

A

5-HT2a and 5-HT2c; one or both of these receptor subtypes may play a role in the subjective and behavioral effects

52
Q

5-HT2a receptor activation

A

is the critical mechanism of action of the compounds in producing hallucinatory experiences in humans

53
Q

how does salvinorin A exert effects?

A

has little/no effect on 5-HT receptors, but is a potent agonist at the k-opioid receptor; little is known about how it produces its hallucinogenic effects

54
Q

neural mechanisms underlying hallucinogenesis

A

activation of 5-HT2a receptors enhances glutamate-mediated excitation of pyramidal neurons in layer V of the prefrontal cortex; this excess glutamate is being released from thalamocortical afferents which interferes with thalamic filtering of sensory information being sent to the cortex

55
Q

what are hallucinogenic drugs hypothesized to interfere with?

A

the normal gating or screening of sensory information passing through a circuit that includes the prefrontal cortex, thalamus, and striatum

56
Q

withdrawal and dependence

A

do not produce physical withdrawal after chronic use; are not reinforcers in animals; some evidence for dependence/tolerance in people

57
Q

dependence

A

a hallucinogen dependence syndrome has been identified in some individuals with early exposure

58
Q

tolerance

A

most produce rapid tolerance with repeated use; down regulation of 5HT-2a may underly tolerance;

59
Q

bad trip

A

related to an interaction between the drug, the individual’s emotional state going into the trip, and the external environment

60
Q

PCP as an anesthetic

A

produces an unusual anesthesia; people show no responsiveness to painful stimuli, but they are not in a typical state of relaxed unconsciousness, but instead exhibited a trance-like or catatonic-like state characterized by a vacant facial expression, fixed and staring eyes, and maintenance of muscle tone

61
Q

why was PCP initially thought to be clinically promising?

A

because it did not produce the respiratory depression associated with barbiturate anesthesia

62
Q

post operative reactions to PCP

A

blurred vision, dizziness, mild disorientation, hallucinations, severe agitation, violence

63
Q

why did ketamine get produced?

A

as a safer version of PCP; is less potent and shorter acting

64
Q

what can PCP and ketamine be considered?

A

anestetic agents

65
Q

what form does PCP come in?

A

powdered or pill form and can be ingested throughout any common route

66
Q

what form does ketamine come in?

A

it is marketed as an injectable liquid, but street sellers evaporate it to yield a powder that is either snorted directly or compressed into pill form

67
Q

effects of subanestetic dose of PCP

A

feeling detached from their body, vertigo, floating, numbness, dream-like state, drowsiness, apathy, loneliness, negativism, hostility, cognitive disorganization, difficulty maintaining attention, deficiencies in abstract thinking, halting speech

68
Q

effects of low doses of ketamine

A

results similar to those of PCP

69
Q

doses of ketamine in the anesthetic range

A

people lose all mental contact with their environment for 10+ minutes–> dissociative anesthesia

70
Q

role of NMDA for both ketamine and PCP

A

is the principle molecular target; noncompetative antagonists at the NMDA receptor complex; binds inside the receptor’s ion channel

71
Q

NMDA

A

ionotropic receptor for the excitatory amino acid neurotransmitter glutamate; widely distributed in the brain (cerebral cortex, hippocampus) and play a role in glutamate signaling

72
Q

noncompetative antagonists at the NMDA receptor complex

A

they block the receptor at a site different from the site at which glutamate or NMDA binds

73
Q

what side effect does NMDA play a role in for PCP and ketamine?

A

cognitive deficits; increased presynaptic glutamate release within the cortex –is a secondary consequence of NMDA receptor antagonism; increased glutamate activity in the anterior cingulate cortex is associated with psychotic symptoms

74
Q

are PCP and ketamine addictive?

A

both are very reinforcing

75
Q

reinforcing effects of PCP and ketamine

A

both activate midbrain DA cell firing and stimulate DA release in the prefrontal cortex; however, there are both DA and non-DA mechanisms underlying reinforcing effects

76
Q

can you produce dependence/tolerance for ketamine?

A

yes-

77
Q

antitussives

A

medications that suppress the cough reflex

78
Q

adverse effects of chronic ketamine use

A

urological symptoms (bladder pain, incontinence), memory deficits, delusional thinking, gray and white matter abnormalities, increased D1 receptor binding in the prefrontal cortex, which may be the result of decreased presynaptic DA transmission

79
Q

adverse effects of chronic PCP use

A

decreased NMDA receptor binding, reduced number of symmetrical spine synapses in the prefrontal cortex, apoptotic cell death in the developing brain

80
Q

effects of chronic PCP and ketamine use in monkeys

A

reduction in tyrosine hydroxylase immunoreactivity (used as a marker of DA axons and terminals)

Behavioral Pharmacology (11 decks)

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