Methyllycaconitine citrate

112825-05-5

C43H58N2O17

DMSO : 250 mg/mL (285.74 mM; Need ultrasonic and warming); H2O : 2.18 mg/mL (2.49 mM; Need ultrasonic and warming)

Neuronal Signaling; Membrane Transporter/Ion Channel

Methyllycaconitine citrate is a specific antagonist of alpha7 neuronal nicotinic acetylcholine receptor (alpha7nAChR). IC50 & Target: alpha7nAChR^[1] In Vitro: Pretreatment with 5 and 10 uM Methyllycaconitine citrate (MLA) inhibits the decreased cell viability induced by Abeta_25-35. Cell viability does not decrease after exposure to Methyllycaconitine citrate (2.5, 5, 10, 20 uM). Abeta_25-35 treatment increases LC3-II levels, which is inhibited by administration of Methyllycaconitine citrate. Methyllycaconitine citrate also inhibits Abeta-induced autophagosome accumulation in SH-SY5Y cells. Flow cytometry also demonstrates decreased MDC-labeled vacuoles with Methyllycaconitine citrate treatment^[1]. In Vivo: Methyllycaconitine citrate (MLA) (6 mg/kg) given alone intraperitoneally does not cause climbing behavior when compare with the saline group. Pretreatment with Methyllycaconitine citrate significantly inhibits methamphetamine (METH)-induced climbing behavior, by about 50%. Methyllycaconitine citrate does not modify either basal locomotor activity or METH-induced hyperlocomotion. The METH-induced depletion of dopamine neuron terminals is attenuated in mice pretreated with Methyllycaconitine citrate (250+/-43 fmol/mg, n=7). A direct effect of Methyllycaconitine citrate on body temperature is ruled out because Methyllycaconitine citrate does not affect basal body temperature (37.0+/-0.5C, n=5) or reduce the METH-induced hyperthermia (38.2+/-0.4C, n=6, MLA+METH group, n.s. versus METH group)^[1].