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PCTH 325 > Psychedelics > Flashcards

Psychedelics Flashcards

1
Q

What does ‘psychedelic’ mean?

A

‘mind manifesting’ in Greek

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2
Q

How are psychedelics classified (2)?

A
  1. Classical (Serotonergic) Psychedelics
  2. Non-classical (Non-) Psychedelics
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3
Q

What are the properties of classical psychedelics + 4 examples?

A

-structural similarities to serotonin
-activates serotonin 2A receptors
-similar but unique effects on cognition, perception, sensory processing
-Psilocybin, LSD, DMT, mescaline

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4
Q

What are the properties of non-classical psychedelics +2 examples

A

-structurally dissimilar to serotonine
-don’t activate serotinin 2A receptors
-alterations in cognition, perception, sensory processing
-Ketamine, MDMA

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5
Q

MOA and effects of Ketamine and MDMA

A

Ketamine:
-glutamate NMDAR antagonist that indirectly activates excitatory AMPAR signalling
-dissociative effects
MDMA:
-release serotonin/dopamine via transporters
-stimulant/’ecstasy’ effects

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6
Q

How do psychedelics mainly work?

A

-First pass metabolism in liver (+sometimes GI tract) by cytochrome CYP450 enzymes

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7
Q

Which neurotransmitters are mainly responsible for excitatory vs inhibitory neurotransmission?

A
  1. Excitatory: Glutamate
  2. Inhibitory: GABA
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8
Q

What are the MOA of the main neurotransmitters?

A
  1. Glutamate: activate glutamate AMPA+NMDA receptors -> neuronal depolarization (ON)
  2. GABA: activate GABAA receptors -> neuronal hyper-polarization (OFF)
    Glutamate/GABA: fast ionotropic neurotransmisison via ligand-gated ion channel receptors
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9
Q

What is the neurotransmitter pathway of psychedelics?

A

Neuromodulators: Serotonin (5HT) Dopamine (DA), Norepinephrene (NE)

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10
Q

What type and MOA of receptor is used for neuromodulators?

A

G-coupled protein receptors (GPCR)
-associated w/ slower changes in intracellular signalling
1. NT binds
2. G-protein activated
3. G-protein subunits or intracellular messengers modulate ion channels
4. Ion channel opens
5. Ions flow across membrane

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11
Q

Which specific neuromodulators do classical psychedelics target?

A

Activates 5-HT receptor subtypes (mainly 2A) of serotonin
Partial agonists (not as effective as 5HT)

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12
Q

What are the 2 signalling pathways of classical psychedelics?

A
  1. 5HT2A canonical signaling
    -excitatory, Gq-coupled
    -prolonged activation recruits B-arrestin -> desensitization, internalizaiton, degradation -> drug tolerance
  2. Non-canonical signalling
    -arrestin-bound receptors regulate unique downstream cascades (cell growth, proliferation, angiogenesis)
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13
Q

How is serotonin activity terminated?

A
  1. Monoamine oxidase: removes serotonin (5HT) from synapse following release via neurotransmission/psychedelic activation
  2. 5HT reuptake from synapse: by specific monoamine transporter, SERT
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14
Q

What are the causes of major depressive disorder (MDD)?

A

-monoamines (serotonin deficiency)
-genetics, stress
-emerging theories (impaired glutumate neuroplasticity)

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15
Q

What is an emerging psychedelic treatment for depression?

A

Ketamine: clinical discovery that low-dose has robust antidepressant effects (hrs to weeks)

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16
Q

What are the 3 neuroplasticity processes at excitatory synapses?

A
  1. Neurogenesis (rare in adults)
  2. Synaptic plasticity
  3. Structural plasticity
17
Q

What is synaptic plasticity?

A

Activity dependent strengthening/weakening of:
1. synaptic transmission
2. long-term potentiation (LTP)
3. long-term depression (LTD) - cell substrates of learning/memory in the brain)

18
Q

What is structural plasticity?

A

Physical modifications of:
-axonal/dendritic branches
-spine morphology
-synaptic numbers that mediate adaptations to environmental stimuli (learning events, pathophysiological processes) via synaptogenesis/synaptic atrophy

19
Q

What is the major site of pathogenesis?

A
  1. Medial prefrontal cortex (mPFC)
  2. Hippocampus (HPC)
20
Q

Explain the pathogenesis of depression

A

Stress/Susceptibility -> Dysregulated synaptic/neural plasticity-> Maladaptive regional sturctural plasticity+ altered neurocircuit activity/connectivity, neuronal atrophy -> depression symptoms (altered stress response, cognition, emotion)

21
Q

What is the mechanism of ketamine and classical psychedelics in neuroplasticity?

A

Promote synaptic homeostasis and adaptive rewiring of pathological circuitry -> Reversal of stress-induced structural/function deficits

22
Q

How do neuromodulator neurotransmitter pathways contribute to the therapeutic effects of classical psychedelics?

A

Transient window of increased plasticity
1.Activate 5HT2A receptors -> downstream cascades through GPCR signalling
2.Increased extracellular glutamate release -> neuron excited + synaptogenesis in mPFC/HPC
3. New connections + patters of functional connectivity across the brain
4.Enhanced window of neuroplasticity for adaptive rewiring, structural changes

23
Q

How is the head twitch response used to measure psychedelic drug action?

A

Activate 5-HT2A via acute psychedelic administration increases frequency of rodent head twitch
Over 30 different psychedelics correlated b/w specieis = predictive validity

24
Q

What are important research and clinical considerations of psychedelic therapy?

(key factors, treatment model, major hurdles)

A
  1. Key factors: dose, set, setting
  2. Treatment model: screening, preparation, psychedelic-assisted therapy, integration, reporting
  3. Major hurdles: funding, regulations, methods, ethics, stigma
25
Q

What are some current psychedelic research limitations?

A

-small cohorts/sample size
-mostly short-term studies
-no gold standard for placebo control
-recruitment bias
-cost/access/equity/scalability
-appropriate safety assessments
-appropriate efficacy endpoints

26
Q

Why are psychedelics considered non-addictive?

A

-tolerance/cross-tolerance (decreased drug effects w/ repeated use)
-use patterns (sporadic/recreational)
-long-lasting ‘trip’
-potential modulation of limbic system (5HT2A activation causes changes in phasic dopamime release -> affect rewarding aspects of drug abuse)

PCTH 325 (19 decks)

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