🧵"Psychoplastogens" = drugs that rapidly induce physical changes in the brain (neuroplasticity).
Examples: ketamine, psilocybin, LSD, DMT, MDMA.
Neuroscientists can literally watch new connections sprout overnight, as in the example below.
Movie:
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There are other plasticity-promoting psychoactive drugs, such as SSRIs, that are not psychoplastogens because they induce plasticity on a slower time scale (weeks).
Psychoplastogens can stimulate plasticity when exposed to neurons for <1 hour.
I first learned about this term from the work of @DEOlsonLab.
I discussed his research with him in a recent podcast conversation, including his work on #psychedelics like ibogaine.
Listen here:
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I have discussed other psychoplastogens, like #psilocybin, with neuroscientists like @kwanalexc.
In that conversation, Dr. Kwan shared some fascinating microscopy videos of neurons in mice.
Watch here:
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I also learned about ketamine, and how it compares to traditional depression medications like SSRIs, in a conversation with @LisaMonteggia:
Listen here:
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🧵#ScienceBreakdown: "Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors"
Interesting new paper by @DEOlsonLab, @LinTianPhD, et al. looking at why some serotonin 2A receptor agonists promote neuroplasticity, but others do not.
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Various small molecules, from endogenous neurotransmitters like serotonin to tryptamine #psychedelics, activate 5HT2A receptors... and yet they can lead to very different effects.
Getting at why this is was one of the basic motivations for this study.
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One idea here is that various compounds have distinct physical/chemical properties, despite all activating 5HT2A receptors.
For example, they differ in fat solubility. Some can cross cell membranes to get *inside* cells, and some can't...
🧵I've done several episodes about #COVID, including the origins of the #SARSCoV2, the biological & epidemiology of the virus, and how mRNA vaccines work.
Here are a few good ones, and a long-from article, that focus on these topics:
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"The Mystery of SARS-CoV-2 & the Origins of COVID-19" with @Ayjchan:
"Death and psychedelics: How science is reviving this ancient connection"
Explores the relationship between #psychedelics & death. It integrates the perspective of thinkers ranging from Timothy Leary to Aldous Huxley to @BrianMuraresku.
Inspired by convos w/ scientists like David Nichols, @DEOlsonLab & others, explores the question of whether #psychedelics subjective effects are required for any of their therapeutic benefits.
Just learned that fluvoxamine, a common SSRI used to treat depression and other psychiatric conditions, increases the half-life of caffeine in the bloodstream.
Like, to an absurd degree:
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Fluvoxamine does this by inhibiting a cytochrome P450 enzyme that metabolizes caffeine. Caffeine levels remain elevated for way longer than normal.
This would be bad for sleep.
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When people feel tired from sleep disruption, they often naturally use more caffeine, which can lead to dependency, i.e. you will get withdrawal symptoms if you stop.
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