Methyllycaconitine citrate(MLA) is an antagonist of α7-containing neuronal nicotinic acetylcholine receptors (nAChRs; Ki = 1.4 nM)[1,2].
MLA inhibits the decreased cell viability induced by Aβ25-35, pretreatment with 5 and 10 µM. Aβ25-35 treatment increases LC3-II levels, which is inhibited by administration of Methyllycaconitine citrate. MLA also inhibits Aβ-induced autophagosome accumulation in SH-SY5Y cells.
MLA inhibits methamphetamine(METH)-induced climbing behavior by 50%. MLA prevents a decrease in striatal synaptosome dopamine (DA) uptake, MLA significantly attenuates METH-induced neurotoxicity at 72 h post-treatment. MLA fully prevents microglial activation at 24 h post-treatment and tending to confirm its neuroprotective activity.
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