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PMCOL 305 > Hallucinogens > Flashcards

Hallucinogens Flashcards

1
Q

What are the sources of hallucinogens?

A

Fungi
Animals
Plants

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2
Q

What are forms of fungi hallucinogens?

A

Claviceps purpurea fungus = lyseric acid
200 Psilocybe, Panaeolus, Conobye species = psilocybin
Amanita muscaria = ibotenic acid and muscimol

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3
Q

What is the hallucinogen derived from an animal?

A

Colorado river toad = bufotenin

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4
Q

What forms of hallucinogens come from plants?

A

LA amide
Mescaline
N,N-dimethyltryptamine, harmine, harmaline
DMT, bufotenin
Atropine, scopolamine, hyoscyamine
Ibogaine
Myristicin, elemicin

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5
Q

What drug is derived from Ipomoea nil seeds?

A

LA amide

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6
Q

What drug is derived from Lophophora williamsii (peyote)?

A

Mescaline

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7
Q

What drugs are derived from Ayahuasca?

A

DMT, harmine, harmaline

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8
Q

What drugs are derived from Anadenanthera peregrine and Virola trees?

A

DMT and bufotenin

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9
Q

What drugs are derived from Atropa belladona, Datura, Henbane, and Mandrake?

A

Atropine, scopolamine, hyoscamine

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10
Q

What drug is derived from Tabernatnthe iboga roots?

A

Ibogaine

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11
Q

What drugs are derived from Myristica fragrans?

A

Myristicin
Elemicin

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12
Q

What are the chemical forms of hallucinogens?

A

Indoleamine nucleus
Phenethylamine nucleus
Catechol nucleus
Dissociatives and deliriants

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13
Q

Are all hallucinogens safe?

A

No

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14
Q

What is foundational to accessing the subconscious and avoiding bad trips for medical use?

A

Set and settings

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15
Q

How do we classify psychedelics?

A

Vivid sensations, altered perceptions and reality
User are still responsive, communicative

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16
Q

How do we classify deliriants?

A

Vivid, maybe confusing, fantasy

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17
Q

How do we classify dissociatives?

A

Analgesia, amnesia, catalepsy, detached reality

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18
Q

What are the big 3 effects of hallucinogens?

A

Hallucination = an experience involving the perception of something that may not actually be present
Illusion = altered and distorted perceptions, thoughts, feelings, insights, awareness
Delusion = fixed belief, unchanged by conflicting evidence

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19
Q

What are trips dependent on?

A

Mindset and setting

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20
Q

What is potency like from high to low in hallucinogens?

A

LSD->Mescaline

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21
Q

What do prototypical psychedelic LSD and 5HT21 receptor biology affect?

A

Frontal cortex thought and perception plus locus coeruleus and thalamus

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22
Q

How is LSD administered?

A

Ingested, injected, transdermal

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23
Q

How much LSD is present in one dose?

A

10-300 mg

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24
Q

What tools are used to administer LSD?

A

Blotting paper, sugar cube, gel caps, pressed tablets/microdots

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25
Q

What is microdosing?

A

using sub-psychedelic amounts

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26
Q

What is the onset of LSD?

A

30-90 minutes

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27
Q

How much LSD enters the brain?

A

1%

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28
Q

What is the TI of LSD?

A

> 1000

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29
Q

How is LSD metabolized?

A

By the liver

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30
Q

What is the half-life of LSD?

A

110-175 minutes

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31
Q

What is the duration of an LSD high?

A

5-12 hours

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32
Q

Where does LSD have a high occupation time?

A

5HT2a receptors

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33
Q

What is stage 1 of an LSD trip?

A

0-30 minutes
Physiological changes outside the brain, sympathomimetic, dizziness, nausea, muscle tremors, numbness

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34
Q

What is stage 2 of an LSD trip?

A

30-120 minutes
Alteration of perceptions, familiar objects take on new appearances, time is lengthened, intense colours, patterns/textured illusions, movement in stable objects, intense sounds, smells, tastes, synesthesia

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35
Q

What is stage 3 of an LSD trip?

A

3-5 hours
Illusions continue, perception of self as mind/body disconnect, distorted body appearance, deeper sense of self

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36
Q

What are the psychological effects of LSD intoxication?

A

Visual hallucinations and illusions
Synesthesia
Time and physical distortions
Intense emotion
Mystical, spiritual encounters
Introspection, ego dissolution

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37
Q

What is synesthesia?

A

Overlapping senses, altered thalamic routing

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38
Q

What are the cognitive effects of LSD intoxication?

A

Inability to concentrate/focus, preoccupation with trivial thoughts, impaired judgment, communicating with God or telepathy with other animals

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39
Q

How is LSD sympathomimetic?

A

Increases BP
Vasoconstriction
Sweating
Dilated pupils

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40
Q

What are animal behaviours on LSD?

A

Animals will not self-administer
Animals actually evoke effort to stop administrations

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41
Q

What does LSD activate?

A

D2-like signaling in the NAc and striatum
Not rewarding
May drive hallucinations

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42
Q

What are the physiological mechanisms of LSD?

A

LC fear centre, 5HT21 in other regions projects to LC, augments LC responses to regular events into extremely novel, seemingly new encounters
Thalamus - routing hub for sensations, mixing of inputs and outputs

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43
Q

What is LSD an agonist of?

A

An agonist at 5-HT1A/B, 2A/B/C, 6 and 7; primarily 2A

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44
Q

What are the cellular mechanisms of LSD action?

A

High pre-synaptic expression in the cortex = perception and information processing centres
Controls transcriptional programming even after a single use
Presynaptic in mPFC
Governs neuroplastic changes via glutamate signaling
Complementary actions by other 5HT receptors and DA receptors
High affinity agonist at D2-like receptors, coupled to Gi/o

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45
Q

What part of the receptor structure explains a high occupation time for LSD?

A

L229

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46
Q

What do drug-receptor interactions allow for?

A

Selection of signaling capabilities

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47
Q

How do receptor conformations bias signaling in LSD?

A

Gaq -> PKC and Ca2+ pathways are activated by non-hallucinogenic chemicals
Prolonged receptor occupation shifts activation away from Gaq
Hallucinogens activate beta-arrestin = desensitization/internalization, MAPK pathways

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48
Q

Do hallucinogens evoke positive reinforcement?

A

Not typically
LSD is low on abuse scale potential

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49
Q

What drug may evoke positive reinforcement?

A

Deliriants (muscarinics)
-M2/4 are Gi/o linked
-M5 is Gq linked, elevates intracellular Ca2+

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50
Q

How is psilocybin absorbed?

A

Ingested

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51
Q

What is the duration of psilocybin?

A

3-6 hours

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52
Q

What are some of the effects of psilocybin?

A

Milder version of LSD
No flashbacks, no lethal cases
Sympathomimetic, altered time and perceptions, hallucinations, heightened emotions

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53
Q

What is psilocybin metabolized to and where?

A

Metabolized to psilocin in the gut and liver

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54
Q

What is psilocybin an agonist of?

A

5HT2a

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55
Q

Is psilocybin addictive?

A

Not addictive, rapid tolerance

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56
Q

How is DMT absorbed?

A

Snorted, smoked, or injected

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57
Q

What happens to DMT in the gut?

A

It is destroyed in the gut

58
Q

What could DMT be used to treat?

A

Worms, parasites

59
Q

What is DMT an agonist of?

A

5-HT2A/C and 1A

60
Q

Do we build a tolerance to DMT?

61
Q

What are the physiological effects of DMT?

A

Similar to LSD and psilocybin

62
Q

What are the psychological effects of DMT?

A

Intense, vivid hallucinations, emotions, introspection, connection to surroundings

63
Q

What is found in harmine and harmaline?

A

Beta-carboline chemicals

64
Q

What types of inhibitors are harmine and harmaline?

A

Selective and reversible monoamine oxidase-A inhibitors
Acetylcholinesterase inhibitors

65
Q

What might an acetylcholinesterase inhibitor be useful in treating?

A

Alzheimer’s disease

66
Q

What can harmine and harmaline treat?

A

Parkinson’s due to stimulating striatal DA release at high doses

67
Q

How is DMT protected in Ayahuasca?

A

The MAO inhibitors in the beta-carbolines protect DMT from degradation so there is enhanced distribution in the brain

68
Q

What are the effects of Ayahuasca?

A

Activates vision and memory brain regions
Powerful visions, intense emotion, profound introspection

69
Q

What are the adverse effects of Ayahuasca?

A

Vomiting, diarrhea

70
Q

What is bufotenin chemically similar to?

71
Q

What are the common effects of bufotenin?

A

Drooling, heat palpitations, elevated BP, oxygen depletion, cramped muscles, blurred vision, headache, toad breath

72
Q

What are hallucinations from bufotenin caused by?

A

Decreased oxygen to the optic nerve

73
Q

What else do toads produce?

A

Toxic glycosides that cause dysrhythmias

74
Q

How might ibogaine block addiction circuits?

A

Elevates glial cell line-derived neurotrophic factor in the midbrain
GDNF release in the VTA reduces cravings and drug intake

75
Q

What are the adverse effects of ibogaine?

A

May damage cerebellum, cause severe motor tremors, increase risk of heart attack and seizure

76
Q

How is mescaline absorbed?

77
Q

What is the duration of mescaline?

A

4-12 hours

78
Q

What is the TI of mescaline?

79
Q

What are the effects of mescaline?

A

Vivid hallucinations similar to LSD

80
Q

What are the adverse effects of mescaline?

A

Toxic effects evoke nausea and vomiting
Death due to convulsions and respiratory arrest

81
Q

How are nutmeg and mace absorbed?

A

Ingested, inhaled, insufflated

82
Q

What do low doses (5g) of nutmeg and mace cause?

A

Very mild hallucinations, disorientation, confusion, feelings of unreality, euphoria

83
Q

What do higher doses (5-30g) of nutmeg and mace cause?

A

Hallucinations, facial flushing, dizziness, apprehension, nausea, vomiting
Unreality can persist for days

84
Q

How do you microdose psychedelics?

A

Sub-hallucinogenic doses, 1 day on/2 days off for a few weeks

85
Q

What hallucinogens are used to microdose?

A

Primarily LSD and psilocybin

86
Q

What are the benefits of micro-dosing?

A

Emerging studies support beneficial effects on mood, creativity, outlook

87
Q

What does 5HT underlie?

A

Complex cognitive and emotional functions in humans

88
Q

What does 5HT2a expression in sub-cortical nuclei alter?

A

Functional connectivity = support perception, memory, attention

89
Q

What are some plant-derived anticholinergics?

A

Mondragora officianrum (mandrake)
Atropa belladonna (nightshade)
Datura stramonium (datura)
Hysocyamus niger (henbane)

90
Q

What are the effects of mandrake at low doses?

A

Relieve anxiety, induce sleep

91
Q

What are the effects of mandrake at high doses?

A

Cause hallucinations, amnesia, muscular paralysis

92
Q

What are the 3 primary tropane alkaloids in plant-derived anticholinergics?

A

Atropine, scopolamine, hyoscyamine

93
Q

What types of doses are required for hallucinations from plant-derived anticholinergics?

A

High, near toxic doses

94
Q

What do plant-derived anticholinergics block?

A

Muscarinic AChRs which dilate pupils, increase heart rate, dry secretions

95
Q

What are the physiological effects of anticholinergics?

A

Elevates heart rate, dry mouth, lack of perspiration, constipation, difficultly urinating

96
Q

Why can anticholinergics be fatal?

A

They cause rapid heart rate, hyperthermia, asphyxia

97
Q

Do anticholinergics produce euphoria?

98
Q

What do anticholinergics prevent?

A

ACh-mediated activation

99
Q

What are some forms of dissociatives?

A

Phencyclidine, ketamine anesthetics
Amanita muscaria, Salvia divinorum

100
Q

What are the effects of dissociatives?

A

Completely removed from reality, detached

101
Q

What do dissociatives produce in animal models?

A

Reinforcement
Unique hallucinations but not due to augmented DA release in the NAc

102
Q

How is PCP absorbed?

A

Inhaled, dip a cigarette in free-base and smoke it
Ingested, insufflated, injected

103
Q

What is the duration of PCP?

104
Q

What is the TI of PCP?

105
Q

What are the effects of 5mg of PCP?

A

Anesthetic, analgesic, stimulant, depressant, convulsant, hallucinogen

106
Q

What are the effects of 10mg of PCP?

A

Any combination of muscle rigidity, loss of pain sensitivity, agitation, mood swings, combative, sympathomimetic, visual/auditory hallucinations, detachment

107
Q

What does PCP block?

A

NMDARs in the cortex and hippocampus

108
Q

What does PCP increase the synthesis and release of?

A

DA, causing agitation, stimulation, locomotor activity

109
Q

What effects of PCP may last for days or weeks?

A

Delirium, confusion, paranoia, impaired memory

110
Q

What is a toxic dose of PCP?

A

> 20mg, can cause convulsions, respiratory failure, coma, death

111
Q

What are most PCP deaths linked to?

A

Behaviours while tripping

112
Q

How is ketamine absorbed?

A

Ingested, inhaled, insufflated, injected

113
Q

What is the onset and duration of ketamine?

A

15-20 minute onset
35-60 minute duration

114
Q

What are the effects of ketamine?

A

Same effects as PCP but shorter acting

115
Q

What are the cellular mechanisms of PCP and ketamine?

A

Block the NMDAR ion channel
Affect Glu, NE, DA, ACh, 5-HT neurotransmitters

116
Q

What is dependence on PCP and ketamine like?

A

Moderate risk, mildly reinforcing but no DA increases in the NAc
PCP self-administration in animal models
Mostly psychological, slight physical dependence
Ketamine dependence is linked to access, not neurocheistry

117
Q

What are the adverse effects of PCP and ketamine?

A

Psychosis and analgesia which leads to damaging behaviors
-attempting superhuman feats
Ketamine cystitis
Memory loss, speech problems, delusional thinking

118
Q

What is ketamine cystitis?

A

Arrest bladder cell growth which causes cell death
Causes bloody urine, pain, incontinence

119
Q

How is Amanita muscaria absorbed?

120
Q

What is the onset and duration of Amanita muscaria?

A

30-90 minute onset
Up to 12 hour duration

121
Q

What effects of Amanita muscaria can last for days?

A

Withdrawal headaches, amnesia, sleepiness

122
Q

What happens to the active chemical in Amanita muscaria?

A

Is excreted in the urine unchanged

123
Q

What are the effects of Amanita muscaria?

A

Alter body perception, euphoria, dizziness, vivid hallucinations
Muscle twitches, sweat, salivation, constricted pupils, lowered BP

124
Q

What is muscimol?

A

The GABAaR agonist responsible for most effects

125
Q

What does ibotenic acid do?

A

Binds to NMDARs

126
Q

What is the fatal dose of Amanita muscaria?

A

Around 15 mushroom caps

127
Q

How is Salvia divinorum absorbed?

A

Inhaled, chewed

128
Q

What is the duration of Salvia divinorum?

A

15-120 minute duration

129
Q

What are the effects of Salvia divinorum?

A

Vivid visuals, sensory and time disturbances, detachment and floating through time
Nausea, slurred speech, chills

130
Q

What can a high dose of Salvia divinorum cause?

A

Brain lesions

131
Q

What is Salvinorin A?

A

One of the three non-alkaloid hallucinogens

132
Q

What type of agonist is Salvia divinorum?

A

A potent kappa opioid receptor agonist that causes dysphoric effects, anxiety, fear, and confusion in most cases

133
Q

What are new psychoactive substances?

A

Chemical alteration of existing drugs

134
Q

What are 2-C drugs?

A

5HT receptor agonists, likely other receptors/transports too
Produce hallucinations, stimulant effects

135
Q

What are the adverse effects of 2-C drugs?

A

Seizure, extremity rigidity, lethal

136
Q

What is Bromo-dragonFLY?

A

Benzodifuran

137
Q

What is the duration of Bromo-dragonFLY?

138
Q

What does Bromo-dragonFLY bind to?

A

5HT1 and 2A receptors

139
Q

What does Bromo-dragonFLY cause?

A

Severe vasoconstriction via alpha-adrenergic receptors
Similar effects to LSD

140
Q

Why have there been several Bromo-dragonFLY overdose deaths?

A

Because it has a narrow therapeutic window

141
Q

What are N-benzyl-oxy-methyl drugs?

A

Potent 5HT2a agonists

PMCOL 305 (18 decks)

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