for educational and safety purposes
Every compound in the sci-wiki that affects myelin; the ones you can source are floated to the front, then the reference-only entries. Tap any for the full entry, mechanism, and outlets.
1 sourced · 1 reference
Progesterone (P4; pregn-4-ene-3,20-dione) is an endogenous pregnane steroid hormone best known for its reproductive roles and is the prototypical neuroactive precursor within the neurosteroid system. Although the parent hormone signals principally through classical nuclear progesterone receptors and through membrane-associated receptors such as PGRMC1 and the mPR/PAQR family, most of its rapid effects on neuronal excitability arise only after sequential metabolism to 5-alpha-dihydroprogesterone and then to allopregnanolone, one of the most potent endogenous positive allosteric modulators of the GABA-A receptor (the brain's principal inhibitory chloride channel). Progesterone and its metabolites are synthesized within the nervous system itself, where they regulate myelination, neuronal survival, neuroinflammation, and inhibitory tone. It has been studied extensively as a neuroprotective agent, with strong preclinical support but negative large-scale human trials in acute traumatic brain injury.
5α-Dihydroprogesterone (5α-DHP) is an endogenous neurosteroid and progestogen formed when the enzyme 5α-reductase reduces progesterone at the A-ring of the steroid nucleus, yielding 5α-pregnane-3,20-dione. It occupies the committed first step of the principal neurosteroid pathway, standing between progesterone and allopregnanolone (its 3α-hydroxylated metabolite and one of the most potent naturally occurring positive modulators of the GABA-A receptor, the brain's main inhibitory ion channel). Unlike allopregnanolone, 5α-DHP is itself a high-affinity agonist of the classical (nuclear) progesterone receptor, driving progesterone-responsive gene transcription; in horses it is a fully biopotent progesterone receptor agonist that sustains the second half of pregnancy after circulating progesterone becomes undetectable. It is synthesized in situ within neurons and glia of the central and peripheral nervous systems, where its production rises after nerve injury and falls under chronic stress.