| Hazard Information | Back Directory | [Description]
Methyllycaconitine (MLA) is an antagonist of α7-containing neuronal nicotinic acetylcholine receptors (nAChRs; Ki = 1.4 nM). It is less effective at other nAChRs. MLA is used to selectively evaluate the role of α7-containing nAChRs in signaling pathways. | [Uses]
Methyllycaconitine citrate is a specific antagonist of α7 neuronal nicotinic acetylcholine receptor (α7nAChR) with blood-brain barrier permeability. | [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±0.5°C, n=5) or reduce the METH-induced hyperthermia (38.2±0.4°C, n=6, MLA+METH group, n.s. versus METH group)[1]. | [storage]
Store at -20°C | [References]
[1] Zheng X, et al. Methyllycaconitine alleviates amyloid-β peptides-induced cytotoxicity in SH-SY5Y cells. PLoS One. 2014 Oct 31;9(10):e111536. DOI:10.1371/journal.pone.0111536
[2] Escubedo E, et al. Methyllycaconitine prevents methamphetamine-induced effects in mouse striatum: involvement of alpha7 nicotinic receptors. J Pharmacol Exp Ther. 2005 Nov;315(2):658-67. DOI:10.1124/jpet.105.089748
[3] Lockman PR, et al. Chronic nicotine exposure alters blood-brain barrier permeability and diminishes brain uptake of methyllycaconitine. J Neurochem. 2005 Jul;94(1):37-44. DOI:10.1111/j.1471-4159.2005.03162.x |
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