|作者：||Kim Chea-Ha, Park Soo-Hyun, Sim Yun-Beom, Kim Sung-Su, Jung Jun-Sub, Sharma Naveen, Suh Hong-Won|
1Department of Pharmacology, Institute of Natural Medicine, College of Medicine Hallym University, 39 Hallymdaehak-gil, Chuncheon, Gangwon-do 200-702, Republic of Korea.
|刊名：||The Chinese journal of physiology, 2017, Vol.60 (1)|
|关键词：||CNQX; glucocorticoid; hyperglycemia; kainic acid; spinal; supraspinal;|
|原始语种摘要：||Kainic acid (KA) is a well-known excitatory neurotoxic substance. In the present study, effectsof KA-injected intraperitoneally (i.p.), intracerebroventricularly (i.c.v.) or intrathecally (i.t.) on theblood glucose level were investigated in ICR mice. We found that KA administered intraperitoneally(i.p.), intracerebroventricularly (i.c.v.) or intrathecally (i.t.) increased the blood glucose and corticosteronelevels, suggesting that KA-induced hyperglycemia appeared to be due to increased blood corticosteronelevel. In support of this finding, adrenalectomy causes a reduction of KA-induced hyperglycemia andneuronal cell death in CA3 regions of the hippocampus. In addition, pretreatment with i.c.v. or i.t. injectionof CNQX (6-cyano-7-nitroquinoxaline-2, 3-dione; a non-NMDA receptor blocker)... attenuated thei.p. and i.c.v. administered KA-induced hyperglycemia. KA administered i.c.v. caused an elevation of theblood corticosterone level whereas the plasma insulin level was reduced. Moreover, i.c.v. pretreatmentwith CNQX inhibited the decrease of plasma insulin level induced by KA i.c.v. injection, whereas theKA-induced plasma corticosterone level was further enhanced by CNQX pretreatment. Our results suggestthat KA administered systemically or centrally produces hyperglycemia. A glucocorticoid system appearsto be involved in KA-induced hyperglycemia. Furthermore, central non-N-methyl-D-aspartate receptorsmay be responsible for KA-induced hyperglycemia.|