NEUROPHARMACOLOGY AND NEUROTOXICOLOGYSelective death of cholinergic neurons induced by beta-methylamino-L-alanineLiu, Xiao Qian; Rush, Travis; Ciske, Jennifer; Lobner, DougAuthor Information Department of Biomedical Sciences, Marquette University, Milwaukee, Wisconsin, USA Correspondence to Doug Lobner, Department of Biomedical Sciences, Marquette University, 561 N. 15th Street, Rm 446, Milwaukee, WI 53233, USA Tel: +1 414 288 6569; fax: +1 414 288 6564; e-mail: firstname.lastname@example.org Received 25 August 2009 accepted 5 October 2009 NeuroReport: January 6th, 2010 - Volume 21 - Issue 1 - p 55-58 doi: 10.1097/WNR.0b013e328333dfd5 Buy SDC Metrics Abstract Beta-N-methylamino-L-alanine (BMAA) is a nonprotein amino acid that may be involved in neurodegenerative diseases. It is produced by a large variety of cyanobacteria and is found at high levels in the brains of Alzheimer's disease and amyotrophic lateral sclerosis patients. Although BMAA is clearly a neurotoxin, previous studies using cortical cultures indicated that millimolar concentrations were required to cause toxicity. We tested the toxicity of BMAA in septal cultures containing cholinergic neurons and mesencephalic cultures containing dopaminergic neurons. We found that cholinergic, but not dopaminergic, neurons were selectively vulnerable to BMAA toxicity, with toxicity occurring at 30 μM. The toxicity of BMAA to total septal neurons involved activation of N-methyl D-aspartate receptors, whereas the death of cholinergic neurons was mediated by AMPA/kainate receptors. © 2010 Lippincott Williams & Wilkins, Inc.