Plants produce a variety of compounds which affect the human nervous system. Although their effects on humans have been well studied, their role in plants is poorly understood. One such compound, BMAA [S(+)-beta-Methyl-alpha, beta-diaminopropionic acid], is common to all species of the most ancient, living seed plants, the cycads. BMAA in cycads has been incriminated as the etiological source of Guam’s dimentia, a disease in the South Pacific--manifested often years after exposure, that results in an Alzheimer’s and Parkinson’s disease. In the animal nervous system, BMAA acts upon ionotropic and metabotropic glutamate receptors (iGluRs), which are ligand-gated ion channels that transmit synaptic signals necessary for a variety of functions including vision and memory. It is not known if BMAA has a physiological role in plants; however, genes with high sequence similarity to animal iGluRs have been identified in a number of plant species. We have taken a pharmacological approach to uncover the role of plant glutamate receptor (AtGLR) genes, by examining the effects of BMAA, a cycad-derived iGluR agonist, on Arabidopsis morphogenesis. When grown in the presence of BMAA, Arabidopsis seedlings show a two to three fold increase in hypocotyl length and a significant inhibition of cotyledon opening. The effect of BMAA on hypocotyl elongation is light-specific and can be reversed by the simultaneous application of glutamate, the native iGluR agonist in animals. A genetic screen was devised to isolate Arabidopsis mutants with a BMAA insensitive morphology (bim). When grown in the light on BMAA, bim mutants have shorter hypocotyls then wildtype. Analysis of the bim mutants, as well as the role of BMAA, will be discussed.