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Epilepsia. 1993 May-Jun;34(3):393-407.

Role of brainstem structures in seizures initiated from the deep prepiriform cortex of rats.

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1
Department of Pharmacology, Georgetown University Medical Center, Washington, D.C.

Abstract

Previous studies showed that brainstem seizures can still be evoked after transections that separate forebrain from brainstem. We sought to determine whether forebrain-evoked electrographic seizures require brainstem connections for initiation and generalization. Male Sprague-Dawley rats weighing 295-320 g implanted with epidural electrodes had brain transections placed at the pre-, mid-, or postcollicular level. In experiment 1, the transections were limited to severing the brainstem, sparing the telencephalon laterally; these are referred to as "core" transections. In experiment 2, the transections severed the brainstem and also cut through the lateral telencephalon. These "extended" transections were either (a) bilateral, (b) unilateral (i.e., a hemitransection confined to one hemisphere), or (c) partial (sparing pathways ventral to the pretectal nuclei). All transections were performed under ether anesthesia, and seizures were initiated 3 h later by focal infusion of bicuculline (BIC) into the area tempestas (AT) through a previously implanted guide cannula. In experiment 1, bilateral forebrain electrographic seizures occurred in the complete absence of connections between forebrain and brainstem, showing that the brainstem is not required for forebrain-evoked seizures. In experiment 2, forebrain seizures evoked by BIC in AT were suppressed by bilateral extended transections which interrupted connections between AT and the caudal lateral telencephalon. Under these circumstances, application of carbachol with BIC reinstated the forebrain seizure response. These results indicate that carbachol application served to compensate for loss of an excitatory influence on AT resulting from the severing of connections with the caudal telencephalon. The demonstration of direct projections from entorhinal cortex to AT using Fluoro-Gold tracing together with the finding that extended brain transections caudal to the telencephalon do not suppress focally evoked forebrain seizures provided further support for the notion that AT afferents from the caudal telencephalon regulate the sensitivity of AT to BIC. The present findings provide further evidence that seizure substrates in the forebrain and brainstem are separable and independent.

[Indexed for MEDLINE]

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