Abstract

Introduction

Materials & Methods

Results

Discussion & Conclusion

References

Discussion
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A number of studies have suggested that histamine plays an important role in the pathogenesis of seizure disorders. For example, Scherkl et al. found that histidine increased the threshold for pentetrazol-induced seizures (1). Further evidence of the involvement of histamine has been derived from studies in which drugs that deplete brain histamine have been found to increase the duration of clonic convulsions induced by maximal electroshock (MES) in mice (2). In addition, Shimoda et al. (3) demonstrated that the H₁-receptor antagonist, diphenhydramine increased focal spikes or spike and wave complex in patients with grand mal or petit mal epilepsy. On the other hand, it is generally known that a histamine H₃-receptor is considered to act as an autoreceptor in the central nervous system. Thioperamide and clobenpropit are specific antagonists of histamine H₃-receptors and provide new tools for elucidating the precise functions of histaminergic neurons in the brain (4).

Therefore, the present study was undertaken to clarify the role of the histaminergic neuron system on amygdaloid kindled seizures in rats using some histamine related compounds. Participation of postsynaptic histaminergic receptors in amygdaloid kindled seizures was also studied.

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