Dementia and neurodegenerative diseases in the aging popu lation are ma jorand growing medical and social problems.Dementia has its highest incidence in the popu lation over age, which is the fastest growing age group.By, of the total popu lation is projected to be elderly.Research in the areaof neurotoxicology needs addit ional focus in exploring the special risk factors to neuro tox ic in sult exhibited by ourelderly popu lation. Research in the fieldsof aging and neurodegenerative diseases is in the fore pertiseof the toxicologist needs to be focused on the toxi cokinetic and pha rmacodynam ic actionsof chemicals, drugs, and environmen talagents and the problems they pose to the elderly popu lation. Th is sympos ium focused on the roleof excitatory am ino acids as common med ia torsof neuronalcell dea th in neurological disorders and the aging CNS.Theun ique susceptibility and vulnerabilityof the aged CNS to director indirectacting excitotoxins were highlighted by the speakers and the model systems th atthey use to study these problems.These endogenous am ino acids were known since the early s toproduce mem plied. Since then,otherendogenous substances have been found to be potential excitatory neu. Currently, the studyof the pharmacology, neuro chemistry, and Prucalopride neurotoxicologyof excitatory amino acids is oneofthe most active areas in neuroscience, inc lud ing l X. GLU andASP are cons ide red to be thepredomin HA15 antexcit dateneu rotr an smitters exist. Fourrecep torsub types have been extensively char. This introduct ion will be astart ing po intfor the discussionof someofthese po tentiallinks and will also briefly describe the factors th atcontr ibute to turn rotoxins. GLU is un iqueamongo therneu rotr an smitters in requir ing a re lationsh ip with glia for bo th no rm albiosyn. GLU is a twoedged sword as aneu rotr an smittersince too littleor toomu ch results in functionaland orpa tho log ic consequences. I POSTSYNAPT IC NEU IWN F IG. GLU is syn thesiledfrom GLN hy themito chondri alen zyme.Theexact processes thatlead to neuronal death are multifaceted and complex.GLU efflux can be ca lc iumdependentor independentand involves release from synaptic vesiclesor direct cytosolic release. The re is an approximately I, fold difference between the I mM intracellular concentra tionofGLU and th e I M concentration normally found in the brain extracellular space.Thedissipationof the nor ergy collapse results in the massive releaseof nonneu ro nismof bo th ischemic and hypoxia neuronal death. A numberof postreceptor events occur th atresult in the amplification and expressionof neuronal death. These involve ionic events, energy depletion, ca lc iummed ia ted enzymatic events, and free radical gener rated on in the following sections.A substantial bodyof research has focused on the roleof GLU in aging and neurological diseases.The release mech an isms and biosynthesisofGLU will be briefly reviewed as a starting po intfor the discussionof the roleof GLU in neurodegenerative processes and neuronaldeath.Phos is the ma jorenzymatic pathway in forebrainstruc tures for neu rotransmit terbio stem ASP am ino transferase is import ant. PAG generates bo th GLU and NH, which a re produc ts th atare potentially toxic, and bo th act as powerful endproductinhibitorsof the enzyme.