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[3].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[4].[1]. kalappa b i, sun f, johnson s r, et al. a positive allosteric modulator of α7 nachrs augments neuroprotective effects of endogenous nicotinic agonists in cerebral ischaemia. brit.j.pharmacol, 2013, 169(8): 1862-1878.[2]. ward j m, cockcroft v b, lunt g g, et al. methyllycaconitine: a selective probe for neuronal α-bungarotoxin binding sites. febs lett, 1990, 270(1-2): 45-48 .[3]. zheng x, et al. methyllycaconitine alleviates amyloid-β peptides-induced cytotoxicity in sh-sy5y cells. plos one, 2014, 9(10): e111536.[4]. escubedo e, et al. methyllycaconitine prevents methamphetamine-induced effects in mouse striatum: involvement of alpha7 nicotinic receptors. j pharmacol exp ther, 2005, 315(2): 658-67.
