Given the evidence that the inferior colliculus (IC) and superior colliculus (SC) seem to play key roles in connecting auditory pathways and seizure output pathways in the neuronal network for audiogenic seizures (AS) in rats, we examined Fos activation in GABAergic cells and cells immunopositive for glutamate N-methyl-D-aspartate (NMDA) receptors in the IC and SC following AS using the double-labeling procedure. Generalized tonic-clonic seizures (GTCS), which developed as an advanced form of AS in some of the susceptible rats, induced an increase in Fos expression in three IC substructures-the dorsal cortex of IC (DCIC), central nucleus of IC (CIC), and external cortex of IC (ECIC)-and in one SC substructure, the deep gray layer of SC (DpG). Compared with the rats showing GTCS, rats exhibiting wild running (WR) without proceeding to GTCS showed a different pattern of AS-induced Fos expression. The DpG in the WR animals showed no significant increase in the levels of Fos-like immunoreactivity. The degrees of Fos activation that occurred in GABAergic cells and cells immunopositive for NMDA receptors were similar in the DCIC, CIC, ECIC, and DpG following AS. These results suggest that Fos activation in the DpG is involved in the development from WR to GTCS in AS-susceptible rats. They also provide some evidence that some GABAergic neurons in the IC and SC and glutamatergic afferents (via NMDA receptors) to these structures are activated by AS.
Copyright 2002 Wiley-Liss, Inc.