Deans' stroke musings: Psilocin fosters neuroplasticity in iPSC-derived human cortical neurons

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Monday, June 10, 2024

Psilocin fosters neuroplasticity in iPSC-derived human cortical neurons

But hasn't your doctor already prescribed psilocybin for your stroke recovery? WHY NOT? They are that fucking incompetent?

psilocybin (26 posts to May 2014)

Psilocin fosters neuroplasticity in iPSC-derived human cortical neurons

Psilocin fosters neuroplasticity in iPSC-derived
human cortical neurons
Philipp Koch
Central Institute of Mental Health (ZI), Medical Faculty Mannheim, Heidelberg University
https://orcid.org/0000-0003-3713-8786
Malin Schmidt
Central Institute of Mental Health (ZI), Medical Faculty Mannheim, Heidelberg University
Anne Hoffrichter
Central Institute of Mental Health (ZI), Medical Faculty Mannheim, Heidelberg University
https://orcid.org/0000-0001-6009-7826
Mahnaz Davoudi
Central Institute of Mental Health (ZI), Medical Faculty Mannheim, Heidelberg University
Sandra Horschitz
Central Institute of Mental Health
Thorsten Lau
Central Institute of Mental Health (ZI), Medical Faculty Mannheim, Heidelberg University
Marcus Meinhardt
Central Institute for Mental Health https://orcid.org/0000-0002-5103-0731
Rainer Spanagel
Central Institute of Mental Health
Julia Ladewig
Central Institute of Mental Health (ZI), Medical Faculty Mannheim, Heidelberg University
https://orcid.org/0000-0002-5943-7990
Georg Köhr
Central Institute of Mental Health
Article
Keywords:
Posted Date: June 7th, 2024
DOI: https://doi.org/10.21203/rs.3.rs-4242829/v1

Abstract

Psilocybin is studied as innovative medication in anxiety, substance abuse and treatment-resistant depression. Animal studies show that psychedelics promote neuronal plasticity by strengthening synaptic responses and protein synthesis. However, the exact molecular and cellular changes induced by psilocybin in the human brain are not known. Here, we treated human cortical neurons derived from induced pluripotent stem cells with the 5-HT2A receptor agonist psilocin - the psychoactive metabolite of psilocybin. We analyzed how exposure to psilocin affects 5-HT2A receptor localization, gene expression, neuronal morphology, synaptic markers and neuronal function. Upon exposure of human neurons to psilocin, we observed a decrease of cell surface-located 5-HT2A receptors first in the axonal- followed by the somatodendritic-compartment. Psilocin further provoked a 5-HT2A-R-mediated augmentation of BDNF abundance. Transcriptomic profiling identified gene expression signatures priming neurons to neuroplasticity. On a morphological level, psilocin induced enhanced neuronal complexity and increased expression of synaptic proteins, in particular in the postsynaptic-compartment. Consistently, we observed an increased excitability and enhanced synaptic network activity in neurons treated with psilocin. In conclusion, exposure of human neurons to psilocin might induces a state of enhanced neuronal plasticity which could explain why psilocin is beneficial in the treatment of neuropsychiatric disorders where synaptic dysfunctions are discussed.