Reciprocal inhibition controls the oscillatory state in thalamic networks

The thalamus plays a central role in the genesis of both normal spindle oscillations and pathological absence seizures. Inhibitory connections between neurons of the thalamic reticular (RE) nucleus help to prevent seizures. Much modeling and experimental work has focused on the proposal that intra-RE inhibition shortens RE cell bursts, and that when prolonged bursts occur, they activate GABAB receptors, transforming spindle oscillations into absence seizures. Here, we present an alternative model in which intra-RE inhibition prevents epileptiform thalamic activity by desynchronizing RE cell bursts, rather than by controlling their duration. c © 2002 Elsevier Science B.V. All rights reserved.