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Original Article

Exp Neurobiol 2015; 24(1): 24-30

Published online March 31, 2015

https://doi.org/10.5607/en.2015.24.1.24

© The Korean Society for Brain and Neural Sciences

Intracerebroventricular Kainic Acid-Induced Damage AḀects Blood Glucose Level in d-glucose-fed Mouse Model

Chea-Ha Kim1 and Jae-Seung Hong2*

1Department of Pharmacology, Institute of Natural Medicine, College of Medicine, 2Department of Physical Education, College of Natural Science, Hallym University, Chuncheon 200-702, Korea

Correspondence to: *To whom correspondence should be addressed.
TEL: 82-33-248-2255, FAX: 82-33-254-0916
e-mail: jayshong@hallym.ac.kr

Received: February 6, 2015; Revised: February 23, 2015; Accepted: February 23, 2015

Abstract

We have previously reported that the intracerebroventricular (i.c.v.) administration of kainic acid (KA) results in significant neuronal damage on the hippocampal CA3 region. In this study, we examined possible changes in the blood glucose level after i.c.v. pretreatment with KA. The blood glucose level was elevated at 30 min, began to decrease at 60 min and returned to normal at 120 min after D-glucose-feeding. We found that the blood glucose level in the KA-pretreated group was higher than in the saline-pretreated group. The up-regulation of the blood glucose level in the KA-pretreated group was still present even after 1~4 weeks. The plasma corticosterone and insulin levels were slightly higher in the KA-treated group. Corticosterone levels decreased whereas insulin levels were elevated when mice were fed with D-glucose. The i.c.v. pretreatment with KA for 24 hr caused a significant reversal of D-glucose-induced down-regulation of corticosterone level. However, the insulin level was enhanced in the KA-pretreated group compared to the vehicle-treated group when mice were fed with D-glucose. These results suggest that KA-induced alterations of the blood glucose level are related to cell death in the CA3 region whereas the up-regulation of blood glucose level in the KA-pretreated group appears to be due to a reversal of D-glucose feeding-induced down-regulation of corticosterone level.

Keywords: kainic acid, neuronal cell death, blood glucose, D-glucose-fed model