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Neuropsychopharmacology > Lecture 12: Cannabis, Psychedelics, & MDMA > Flashcards

Lecture 12: Cannabis, Psychedelics, & MDMA Flashcards

(72 cards)

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1
Q

cannabinoid

A
  • originally referred to the family of naturally occurring chemicals found in cannabis
  • now refers to all compounds capable of activating cannabinoids
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2
Q

exogenous cannabinoids

A

produced outside the organism
- phytocannabinoids
- synthetic cannabinoids

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3
Q

phytocannabinoids

A

THC, CBD

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4
Q

synthetic cannabinoids

A

nabilone, dronabinol, K2, spice

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5
Q

endogenous cannabinoids

A

produced inside the organism
- anadamide (AEA)
- 2-arachidonyl glycerol (2-AG)

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6
Q

endocannabinoids

A

endogenous cannabinoids
- lipid molecules that act as NTs by binding to CB receptors

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7
Q

synthesis enzymes for endocannabinoids

A

AEA: N-archidonyl phosphatidylethanolamine (NAPE)
2-AG: diacylglycerol lipase (DAGL)

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8
Q

receptors

A
  • cannabinoid receptor 1 (CB1)
  • cannabinoid receptor 2 (CB2)
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9
Q

CB1 function

A

neuromodulation & plasticity

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10
Q

CB2 function

A

immune regulation

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11
Q

other cannabinoid receptors

A
  • Transient Receptor Potential Vanilloid (TRPV-1)
  • G Protein Receptor 55
  • peroxisome proliferator-activated receptors (PPARs)
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12
Q

TRPV-1 function

A

pain perception, temperature sensing

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13
Q

GPR55 function

A

bone metabolism

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14
Q

PPAR function

A

lipid metabolism & inflammation

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15
Q

degradation enzymes

A

AEA: fatty acid amide hydrolase (FAAH)
2-AG: monoacylglycerol lipase (MAGL)

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16
Q

CB1 location

A

CNS
- most abundant GPCR in the brain

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17
Q

CB2 location

A

immune cells
- throughout periphery & microglia (centrally)

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18
Q

AEA receptor interactions

A
  • higher affinity for CB1 than CB2 receptors
  • partial agonist of CB1
  • almost inactive at CB2
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19
Q

2-AG receptor interactions

A

moderate to low affinity for both CB receptors
- full agonist at both
- up to 1000X higher than AEA levels in CNS

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20
Q

what kind of neurotransmission do endocannabinoids exhibit

A

retrograde neurotransmission
- act as a circuit brake

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21
Q

what does CB1 activation cause

A

reduction in NT release

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22
Q

what does the reduction of release of glutamate (Depolarization Induced Suppression of Excitation, DSE) cause

A

prevents overexcitation & neuronal death

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23
Q

what does the reduction of the release of GABA (Depolarization Induced Suppression of Inhibition, DSI) cause

A

strengthens neuronal connections

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24
Q

what does CB2 activation cause

A

release of pro-inflammatory molecules
- suppresses neuroinflammation

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25
structure & function of CB1 & CB2 receptors
Gi/o coupled GPCRs - inhibition of adenylyl cyclase, cAMP, & PKA - has also coupled w/ Gs & Gq - regulates transcription, synaptic plasticity, & NT release
26
what does Gbeta-gamma cause
modulation of ion channels - crucial for reducing NT release
27
sativa characteristics
energizing, stimulating
28
indica characteristics
sedating, relaxing
29
what are the three categories of compounds in cannabis
phytocannabinoids, terpenes, flavonoids
30
photocannbinoids
plant compounds responsible for psychoactive effects & activation of CB receptors - THC & CBD are the most abundant
31
terpenes
plant compounds responsible for odor & taste
32
flavonoids
plant compounds responsible for color
33
THC characteristics
- psychoactive & intoxicating - responsible for 'high' feeling
34
what receptors does THC bind to
both CB1 & CB2 w/ high affinity but only partial agonism
35
CBD characteristics
- non-psychoactive since it doesn't lead to 'high' feelings, but it is active in the brain/body
36
CBD binding activity
- does not bind CB1 or CB2 directly; acts as a modulator - binds TRPV1 w/ high affinity but weak agonism - binds 5-HT1A w/ low affinity & partial agonism
37
characteristics and timeline of metabolism when inhaling cannabis
- bypasses 1st pass metabolism = rapid absorption into the bloodstream & brain - peak blood THC at 3-10 minutes - fast onset & offset - reported effects w/i seconds & up to 6 hours
38
characteristics and timeline of metabolism when ingesting cannabis
- must go through 1st pass metabolism = slower absorption into blood stream & takes longer to reach the brain - peak blood THC at 1-2 hours - slow onset & prolonged effect - reported effects within 30 minutes & up to 12 hours
39
what are the active metabolites of THC
11-OH-THC, THC-COOH
40
which metabolite of THC is psychoactive
11-OH-THC
41
which metabolite of THC is not psychoactive
THC-COOH
42
which versions of THC are hydroxylated by cytochrome P450 enzymes
THC, and 11-OH-THC
43
which metabolite of THC is oxidized by cytochrome P450 enzymes
THC-COOH
44
which metabolite is metabolized the fastest by inhalation
just regular THC
45
which metabolite is metabolized the fastest by ingestion
THC-COOH
46
how does cannabis affect sleep
- promotes falling asleep, but may worsen quality over time - may be beneficial for people w/ sleep disturbances due to insomnia, chronic pain, or PTSD
47
efficacy of cannabis as a treatment for anxiety
- dose-dependent effects - not enough substantial evidence for THC; effects of CBD seem more promising
48
what properties of cannabis allow it to treat chronic pain
- analgesic properties - anti-inflammatory
49
what studies have shown that cannabis is good for treating chronic pain
- improvements in cancer pain - pain reduction in fibromyalgia - significant neuropathic pain related to surgery
50
composition effect of cannabis on pain treatment
most effects seen with THC alone, or THC in combo with CBD - CBD alone has less effectiveness
51
how does a high concentration of THC affect pain
greatest pain reduction, but also most adverse effects
52
summary of cannabis efficacy in treating pain
- promising evidence - in need of placebo-controlled clinical trials
53
main health concerns for cannabis
- increased risk of mental health conditions - impacts on cardiovascular function - lung damage - development of cannabis use disorder
54
what is the link between cannabis use & development of schizophrenia
entirely correlational w/ no directionality - cannabis likely amplifies the speed & severity of schizophrenia in those already predisposed - genetic risk of schizophrenia predicts cannabis use, not the other way around
55
what causes development of cannabis use disorder
if use is weekly or greater the chance of developing it is about 30%
56
factors that increase risk for CUD
- early age of onset - use of high potency products - frequent, daily use - use of cannabis to manage anxiety or trauma
57
three stages of psychedelic therapy
1. preparation 2. dosing 3. integration
58
what are psychedelic drugs
class of psychoactive substances that induce altered consciousness, changes in perception, thought, emotion, & self-awareness
59
how does psilocybin work
psilocybin (biologically inactive) is converted to psilocin via phosphatase enzymes in intestines, liver, kidneys, & blood
60
psilocin activity at receptors
non-selective agonist of serotonin (5-HT 2A) receptors
61
structure of 5-HT2A receptors
G protein receptor most often coupled to Gq, resulting in downstream effects of increased plasticity (spine formation on glutamatergic cells)
62
psilocin onset
20-50 minutes
63
psilocin peak effects
60-90 minutes
64
psilocin duration
4-6 hours
65
can psilocybin be used to treat depression
yes
66
what is MDMA
a synthetic hallucinogenic drug
67
metabolism of MDMA
immediately in an active form, metabolized by CYP430 enzymes in the liver
68
what is the target of MDMA
interacting with serotonin, dopamine, & norepinephrine transporters - increases reuptake of these NTs
69
MDMA receptor interactions
low-affinity partial agonist of serotonin receptors
70
MDMA timeline of effects
- onset in 30-60 minutes - peak effects at ~2 hours - duration of 8 hours - some effects up to 2 days
71
does MDMA reduce PTSD severity
yes
72
what are the issues with psychedelic trials
- lack of placebo-control - not blinded (participants or experimenters) - expectation bias - standardization of therapy type & training - generalizability of findings (populations have been heterogenous) - limited accessibility

Neuropsychopharmacology (17 decks)

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