This enhancement by sunifiram is associated with an increase inphosphorylation of AMPAR through activation of protein kinase II(CaMKII) and an increase in phosphorylation of NMDAR through activation of protein kinase C α (PKCα). More specifically, sunifiram stimulates the glycine-binding site of NMDAR with concomitant PKCαactivation through Src kinase. Enhancement of PKCα activity triggers to potentiate hippocampal LTP through CaMKII activation.Sunifiram improves cognitive deficits via CaM kinase II andprotein kinase C activation.
2.EnhancingLTP in a bell-shapeddose–response relationship.
3.Sunifiram aids in the release of acetylcholine in the cerebral cortex.
Sunifiram is a synthetic derivative of Piracetam, although due to breaking the pyrrolidone backbone it is no longer in the racetam family of nootropics (yet by being derived from them, it is still commonly associated with this class).
Sunifiram has mechanisms similar to Nefiracetam in the hippocampus, and sunifiram shows anti-amnesiac properties and is a cognitive enhancer. Its anti-amnesiac activity is several orders of magnitude greater (significantly more potent) than piracetam, and preliminary evidence suggests it has a very good safety profile.
This compound is known as an AMPAkine due to exerting most of its actions via the AMPA receptor (one of the three main subsets of glutamate receptors, alongside NDMA and kainate). This enhancement of AMPA function seems to also rely on enhancing signalling via the Glycine binding site of NMDA receptors, although one minimal signalling goes through the NMDA receptor then the benefits on AMPA receptors seem dose-dependent.
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