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Study Shows New Mechanism For How Psychedelics Promote Plasticity

A study published in Nature shows potential new way for how psychedelics act on the brain and promote plasticity
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“New study shows psychedelics promote plasticity by directly binding to BDNF receptor Trk”

 

I’m not gonna lie, I had to Google “BDNF receptor”.

And “Trk”.

Yet despite my understandable ignorance, it seems like we’ve received interesting new research on how psychedelics bind to receptors in the brain. A new study published in Nature posits that psychedelics express their significant antidepressant and neuroplastic effects by binding to receptors of the molecule brain-derived neurotrophic factor (BDNF).

With the serotonin 5-HT2A receptor getting most of the attention in psychedelic science circles, this new data could potentially change how we study psychedelics and develop future compounds. The research also theorizes that the antidepressant effects gained from psychedelics could potentially be separated from the trippy hallucinations.

But I’ll stop before I put my layman’s foot in my mouth — and default to the experts and publishers of the research. See their quotes and tweets below explaining some of the results.

 

We recently reported that pharmacologically diverse antidepressants, including fluoxetine and ketamine, act by binding to TrkB, the receptor for BDNF. Here we show that lysergic acid diethylamide (LSD) and psilocin directly bind to TrkB with affinities 1,000-fold higher than those for other antidepressants, and that psychedelics and antidepressants bind to distinct but partially overlapping sites within the transmembrane domain of TrkB dimers.

 

 

 

And some meme fun from the psychedelic science nerds.

 

 

The post Study Shows New Mechanism For How Psychedelics Promote Plasticity appeared first on Microdose.

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