DEEP PREPIRIFORM CORTEX MODULATES KAINATE-INDUCED HIPPOCAMPAL INJURY

As seizure propagation within limbic structures is mediated in part by a small area of deep prepiriform cortex (area tempestas), we investig ated the role of area tempestas in modulating hippocampal injury induc ed by systemic kainate administration. Injury was quantitated by count ing the numbers of neurons that stained for the 72,000 mol. wt heat sh ock protein and with acid-fuchsin dye. Status epilepticus induced thes e markers of neuronal injury in the CA1 and CA3a regions of the hippoc ampus, thalamus, piriform cortex and the amygdaloid complex. Microinje ction of 2-amino-7-phosphonoheptanoic acid, a competitive antagonist o f the N-methyl-D-aspartate subclass of the glutamate receptor, into ar ea tempestas prior to systemic administration of kainate attenuated bo th heat shock protein induction and acid-fuchsin labeling in CA1 and C A3a pyramidal neurons without reducing the duration of electrographic seizures. Injections of bicuculline, a GABA antagonist, into area temp estas produced hippocampal damage when given with subcytotoxic doses o f intravenous kainate. Thus, area tempestas may be a uniquely sensitiv e anatomical structure involved not just in seizure propagation but al so in modulating the extent and pattern of damage induced in hippocamp al neurons as a result of prolonged, systemically induced seizures. Th ese effects are due in part to excitatory and inhibitory projections t o neurons in area tempestas.