Lecture 7 Flashcards

1
Q

examples of psychedelics

A

Psilocybin: mushroom
DMT; plants in america
LSD
Mescaline: cactus
5-MEO DMT: toad

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2
Q

LSD

A

discovre by Albert Hoffman, on accident.
non toxic, non addictive, effective clinical tools. understanding of mental illness: models psychosis. psychological transformation in psychotherapy. Even contacted to Steve Jobs for funding LSD research

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3
Q

why was lsd such a profound founding

A

for neurotransmitters in the brain, especially serotonine

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4
Q

Why was there a lot ophef about lsd?

A

1960s contra culture, vietnam war- anti military attitudes
1971 controlled substances act –> illegal
thought it had something to do with psychosis

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5
Q

Name the three types of psychotropic effects?

A
  • mood : high arousal, mood
  • perception: geometric visual patterning, morphing, abstract imagery
  • cognition: unconstrained cognition, dream like states, loss of ego, loss of sense of self, divine spiritual presence
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6
Q

glutomate

A

mmemory

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7
Q

gaba

A

eating-sleeping- agression

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8
Q

acetychloline

A

movememnt control, thninking

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9
Q

receptor distribution

A

location of the receptors play a role in what we experience!

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10
Q

drugs, what do they do

A

drugs interfere with the way neurons receive, and process signals via neurotransmitters. they lead to abnormal messages being sent through the network

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11
Q

5ht-2a receptors

A

2a affinity & potency
- 2 a antagonist attentuates key psychological efect
- too much serotonin –> receptor down regulation (taking too man y psychedlics in a row - overstimulated)
- cross tolerance - common mechanism

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12
Q

cross tolerance

A

receptor down regulation (taking too man y psychedlics in a row - overstimulated), redce symptoms of anxiety (temporary effect). less intake of serotonin (its same for every psychedelic)

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13
Q

deficient 5-ht2ar-stim

A

preservation (repeating)

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14
Q

increase 5-ht2ar-stim

A

increase sensitivity to environment, lsd makes rats more flexible for example & rapid learners
so it stimulates neurplasticity in the hippocampus and the neocortex, facilitates change/flexibility

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15
Q

5-HT1A and 5-HT2A

A

two most prevalent serotonin receptors

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16
Q

SSRI

A

act on 1A receptors, limbic system. Your limbic responsitivity goes down, so your stress, impulsitivity, agression and anxiety goes down as well, tolerance, resilience, patience and tolerance of stress go up. so your depression goes down and your well being goes up. hopefully.

17
Q

ssri via 5-HT-2A

A

chaos in the brain –> rigid thinking and pessisism goes down, plasticity goes up, environmental sensitivity, learn better and adaptability.change goes up

18
Q

SSRIs vs psychedelics

A

passive vs active coping

19
Q

4 basic mechanisms of 2a serotonin

A
  • increase anxiety acute experience: decreases defenses facilitate emotional approach during therapy, yet less inhibition of emotions and memories
  • emotions bubble up during psychedelic experience
  • 5-HT2AR agonism stimulate neuroplasticity in the hippocampus and the neocortex, associated with flexibility and learning
  • 2A signaling downregulates 5-HT2AR receptors and thus –> less anxiety and improved general well-being during the post acute afterglow
20
Q

fMRI psilocybin study, with 15 volunteers in resting stand. what can we conclude

A

decreases in high level association areas such are hubs in het Default main network: pcc, acc, medial PFC, Thalamus. you would think it would increase but no!
the networks that make sense of the wolrd, they don’t work anymore. It looks fragmented.

desynchronization: default network correlates with ego dissolution, because it’s about having the sense of the self and thinking about yourself in terms of with others

21
Q

Default mode Network (DMN)

A
  • metabolically hungryL 40% more blood than other structure
  • highly interconnected: transit hub/integration centre
    activated in self-reflection, mental time travel, metacognition

–> self/ego

22
Q

Disintegration in connectivity among hub structures meansl…

A

More flexible neurological traffic among the whole brain, cross talk among regions

23
Q

What can we conclude from the study that was preregistered? and psychedelic microdosing and emotion go and no go task?

A

There was no significant difference. Psilocybin microdosing did not affect emotion processing or symptoms of anxiety and depression compared to placebo

24
Q

How can we explain discrepencies?

A
  • no control over the dosis that participant used?
  • baseline levels of emotional well-being were already at sufficient levels such that psychedlelic drug could not improve that much more
25
Q

increasing number of clnical trials

A
  • stopped smoking (80%) after 6 months
  • same goes for drinking
    r- reuced OCD
  • decrease anxiety at 12 months in patiens life threatening illness
  • openess to experience
26
Q

treatment of depression with psychedelics. Thoughts?

A

no good control group, combined therapeutic interventions, low sample sizes. but more recent research seems to replicate these findings

27
Q

how do depression and psychedelics work?

A

depression menas increase focus on self - increase activity and functional connectivity in DMN and decrease focus on external world - in depression low social interaction

–> psilocybin/LSD temporarily disintegrate the DMN during acute intoxication, which reduces self focus

28
Q

what more can psilobycin do?

A

reduced activation of pain regions during social exclusion task, increased emotional empathy and feeling of connection

29
Q

what is the mediating factor for long lasting chance in the quality of life?

A
  • insight
  • mysticism
  • feeling of unity