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.

Thursday, May 11, 2023

Taking a “trip” inside the cell: New research shows how psychedelics promote neuroplasticity

 

Your doctor should already be well versed in mushrooms and micro-dosing. If not, you don't have a functioning stroke doctor. Which means your doctor is woefully inadequate in neuroplasticity, your main means to recovery

Taking a “trip” inside the cell: New research shows how psychedelics promote neuroplasticity 

Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors

Maxemiliano V. Vargas https://orcid.org/0000-0002-3637-1896, Lee E. Dunlap https://orcid.org/0000-0002-9365-8025, Chunyang Dong https://orcid.org/0000-0002-4820-4454, Samuel J. Carter https://orcid.org/0000-0002-2276-4373, Robert J. Tombari https://orcid.org/0000-0002-6561-8181, Shekib A. Jami https://orcid.org/0000-0001-5478-1963, Lindsay P. Cameron https://orcid.org/0000-0002-8420-7898, Seona D. Patel https://orcid.org/0000-0001-8947-4533, Joseph J. Hennessey https://orcid.org/0000-0003-0981-4695, and David E. Olson https://orcid.org/0000-0002-4517-0543 Authors Info & Affiliations
Science
16 Feb 2023
Vol 379, Issue 6633
pp. 700-706
DOI: 10.1126/science.adf0435

    • The mechanism underlying psychedelic action

    Psychedelic compounds promote cortical structural and functional neuroplasticity through the activation of serotonin 2A receptors. However, the mechanisms by which receptor activation leads to changes in neuronal growth are still poorly defined. Vargas et al. found that activation of intracellular serotonin 2A receptors is responsible for the plasticity-promoting and antidepressant-like properties of psychedelic compounds, but serotonin may not be the natural ligand for those intracellular receptors (see the Perspective by Hess and Gould). —PRS

    Abstract

    Decreased dendritic spine density in the cortex is a hallmark of several neuropsychiatric diseases, and the ability to promote cortical neuron growth has been hypothesized to underlie the rapid and sustained therapeutic effects of psychedelics. Activation of 5-hydroxytryptamine (serotonin) 2A receptors (5-HT2ARs) is essential for psychedelic-induced cortical plasticity, but it is currently unclear why some 5-HT2AR agonists promote neuroplasticity, whereas others do not. We used molecular and genetic tools to demonstrate that intracellular 5-HT2ARs mediate the plasticity-promoting properties of psychedelics; these results explain why serotonin does not engage similar plasticity mechanisms. This work emphasizes the role of location bias in 5-HT2AR signaling, identifies intracellular 5-HT2ARs as a therapeutic target, and raises the intriguing possibility that serotonin might not be the endogenous ligand for intracellular 5-HT2ARs in the cortex.
    Related Perspective
    Possible psychedelic therapeutic mechanism
    By Evan M. Hess, Todd D. Gould

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