Pharmacologic blockade of non-NMDA receptors at deep prepiriform cortex attenuates heat shock protein expression in global ischemia.

Deep prepiriform cortex modulates excitatory activity in the limbic system during seizures. We therefore studied a potential role for this system in another process involving excitatory neurotransmission: global ischemia in the rat. The non-NMDA antagonist NBQX was microinjected bilaterally into deep prepiriform cortex prior to 10 min of global ischemia. Hippocampal cell injury was then assessed by heath shock protein (HSP) expression 24 h after ischemia. NBQX significantly decreased the number of HSP positive cells in both CA1 and CA3 hippocampal subsectors, suggesting the possibility that pathways from deep prepiriform cortex to hippocampus modulate excitotoxicity in target neurons during ischemia.