Abstract

Various models of acute experimentally-induced epilepsy indicate that aminergic neurons are involved. It has been demonstrated that a decrease in the level of norepinephrine can increase the susceptibility to epileptic seizures. The present research was undertaken in order to study alterations in the cortical noradrenergic system during the evolution of a chronic epileptic model induced by application of metallic cobalt on the sensorimotor cortex in the rat. The alterations were studied by means of the glyoxylic histochemical fluorescence method combined with biochemical analysis of cortical norepinephrine content. This histochemical and biochemical approach revealed a decrease in the density of noradrenergic terminals in the perifocal area. This decrease corresponds to a significant drop in the norepinephrine level, before the onset of spiking activity. Noradrenergic fiber density was still low and the norepinephrine level was lowest when the first epileptic discharges were recorded. At the end of the epileptic syndrome, sprouting of noradrenergic fibers into the perifocal area coincided with an increase in the norepinephrine level. Thus, this study gives further support to the hypothesis that noradrenergic system is involved in epileptogenesis.

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