A Possible Mechanism of Blocking of Limbic Motor Seizure Reactions Induced by Activation of the Thalamic Reticular Nucleus

Abstract

Experiments were directed toward elucidation of the role of the thalamic reticular nucleus (R) in the modulation of generalized seizure reactions under kindling conditions and of the mechanisms mediating the effects of stimulation of the above nucleus on seizure activity. It was shown that activation of the thalamic R in rats limits generalization of the seizure reactions both in the course of development of seizures of limbic genesis (evoked by stimulation of the hippocampus) and under conditions of the existence of a pre-formed epileptic nidus. Tetanic stimulation of the R in cats under conditions of acute experiments induced significant facilitation of IPSPs in thalamo-cortical neurons of the ventrolateral thalamic nucleus. This effect is rather long-lasting and may be considered a mechanism providing blocking of generalized seizures under kindling conditions.

Enhanced Synaptic Vesicle Traffic in Hippocampus of Phenytoin-Resistant Kindled Rats

“…These results indicated that There were only few animal models of pharmacoresistant epilepsy. Phenytoin-resistant amygdaloid-kindled Wistar rats were the most widely used models for complex partial seizures and for investigating mechanisms of intractable epilepsy, particularly because of an excellent correlation between activity of anticonvulsant drugs in this model and the clinical efficacy against complex partial seizures [7,[13][14][15]. The behavior of kindling rats suggested that this model simulated the complex partial seizures and the process of epilepsy genesis.…”