Recent studies suggest that the deep layers of superior colliculus (DLSC) play a role in the network for audiogenic seizures (AGS) in genetically epilepsy-prone rats (GEPR-9s). The present study examined the role of glutamatergic and noradrenergic receptors in DLSC in modulation of AGS susceptibility. The study examined effects of a competitive NMDA receptor antagonist [dl-2-amino-7-phosphonoheptanoic acid (AP7)] or an alpha1 noradrenergic agonist (phenylephrine) focally microinjected into DLSC as compared to effects in the inferior colliculus (IC) and pontine reticular formation (PRF), which are major established components of the AGS network. The results demonstrated that blockade of NMDA receptors in DLSC suppressed AGS susceptibility. AP7 microinjection was effective at relatively low doses in IC, but required higher doses in DLSC and PRF. The DLSC was relatively more sensitive to seizure reduction by the alpha1 noradrenergic agonist as compared to the IC and PRF. The anticonvulsant effect of AP7 was longer-lasting than phenylephrine in the DLSC and IC but not in the PRF. These data suggest that neurons in the DLSC are a requisite component for the neuronal network for AGS in GEPR-9s and that NMDA and alpha1 adrenoreceptors in this site may play important roles in the modulation of AGS propagation. The relatively greater sensitivity of DLSC to phenylephrine as compared to IC and PRF indicates that norepinephrine may be more important in the modulation of AGS in DLSC, which contrasts to the role of glutamate modulation. These data support recent neuronal recording data, which indicate that DLSC neurons play a critical role in AGS.
Copyright 1999 Elsevier Science B.V.