Development of Amygdaloid Kindling in Histidine Decarboxylase-deficient and Histamine H1 Receptor-deficient Mice

Tadashi Hirai, Chihiro Okuma, Chie Harada, Mitsunobu Mio, Hiroshi Ohtsu, Takeshi Watanabe, Chiaki Kamei

Research output: Contribution to journalArticle

28 Citations (Scopus)

Abstract

Purpose: This study attempted to clarify the role of histamine or histamine H1 receptors in the development of amygdaloid kindling by using histidine decarboxylase (HDC)-deficient and histamine H1 receptor (H1R)-deficient mice. Methods: Under pentobarbital anesthesia, mice were fixed to a stereotaxic apparatus, and bipolar electrodes were implanted into the right amygdala. Electrodes were connected to a miniature receptacle, which was embedded in the skull with dental cement. A bipolar electroencephalogram was recorded; bipolar stimulation of the amygdala was applied every day with a constant-current stimulator and continued until a generalized convulsion was obtained. Results: The development of amygdaloid kindling in HDC-deficient and H1R-deficient mice was significantly accelerated compared with that in their respective wild-type mice. In addition, the afterdischarge (AD) duration and generalized seizure duration in HDC-deficient and H1R-deficient mice were prolonged. Intraperitoneal injection of histidine resulted in an inhibition of amygdaloid kindled seizures in wild-type mice at doses that caused an increase in the histamine contents of the brain. However, no significant effect was observed with histidine in H 1R-deficient mice at the same dose. Conclusions: These findings suggest that histaminergic mechanisms through H1 receptors play a crucial role not only in amygdaloid kindled seizures but also in the development of amygdaloid kindling.

Original languageEnglish
Pages (from-to)309-313
Number of pages5
JournalEpilepsia
Volume45
Issue number4
DOIs
Publication statusPublished - 2004 Apr

Keywords

  • Amygdaloid kindling
  • Histamine
  • Histamine H receptor-deficient mice
  • Histidine
  • Histidine decarboxylase-deficient mice

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

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