| First Author | Hirai T | Year | 2004 |
| Journal | Epilepsia | Volume | 45 |
| Issue | 4 | Pages | 309-13 |
| PubMed ID | 15030492 | Mgi Jnum | J:128979 |
| Mgi Id | MGI:3768459 | Doi | 10.1111/j.0013-9580.2004.19303.x |
| Citation | Hirai T, et al. (2004) Development of amygdaloid kindling in histidine decarboxylase-deficient and histamine H1 receptor-deficient mice. Epilepsia 45(4):309-13 |
| abstractText | 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 H1R-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. |
