Regulation of Blood Glucose Level by Kainic Acid in Mice: Involvement of Glucocorticoid System and Non-NMDA Receptors

10.4077/CJP.2017.BAE397

Chea-Ha Kim；Soo-Hyun Park；Yun-Beom Sim；Sung-Su Kim；Jun-Sub Jung；Naveen Sharma；Hong-Won Suh

CNQX ； glucocorticoid ； hyperglycemia ； kainic acid ； spinal ； supraspinal

The Chinese Journal of Physiology

60卷1期（2017 / 02 / 28）

23 - 31

英文

Kainic acid (KA) is a well-known excitatory neurotoxic substance. In the present study, effects of KA-injected intraperitoneally (i.p.), intracerebroventricularly (i.c.v.) or intrathecally (i.t.) on the blood glucose level were investigated in ICR mice. We found that KA administered i.p., i.c.v. or i.t. increased the blood glucose and corticosterone levels, suggesting that KA-induced hyperglycemia appeared to be due to increased blood corticosterone level. In support of this finding, adrenalectomy (ADX) causes a reduction of KA-induced hyperglycemia and neuronal cell death in CA3 regions of the hippocampus. In addition, pretreatment with i.c.v. or i.t. in-jection of 6-cyano-7-nitroquinoxaline-2, 3-dione; a non-N-methyl-D-aspartate (NMDA) receptor blocker (CNQX) attenuated the i.p. and i.c.v. administered KA-induced hyperglycemia. KA administered i.c.v. caused an elevation of the blood corticosterone level whereas the plasma insulin level was reduced. Moreover, i.c.v. pretreatment with CNQX inhibited the decrease of plasma insulin level induced by KA i.c.v. injection, whereas the KA-induced plasma corticosterone level was further enhanced by CNQX pretreatment. Our results suggest that KA administered systemically or centrally produces hyperglycemia. A glucocorticoid (GC) system appears to be involved in KA-induced hyperglycemia. Furthermore, central non-NMDA receptors may be responsible for KA-induced hyperglycemia.

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