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
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Taking a “trip” inside the cell: New research shows how psychedelics promote neuroplasticity
Psychedelics promote neuroplasticity through the activation of intracellular 5-HT2A receptors
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.
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