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Effects of MK-801 and CNQX on various neurotoxic responses induced by kainic acid in mice.
Mol Cells. 2002 Dec 31; 14(3):339-47.MC

Abstract

Effects of MK-801 (a NMDA receptor blocker) and CNQX (6-cyano-7-nitroquinoxaline-2,3-dione; a non-NMDA receptor blocker) on several neurotoxic responses induced by kainic acid (KA) were examined in ICR mice. In a lethality test, intracerebroventricular (i.c.v.) pretreatment of MK-801 (1 microg), but not CNQX (0.5 microg), attenuated the time to lethality induced by KA (0.5 microg) administered i.c.v. In the memory test (a passive avoidance test), MK-801, but not CNQX, prevented the memory loss induced by KA (0.1 microg). The damage induced by KA (0.1 microg) administered i.c.v. in the hippocampus was markedly concentrated in the CA3 pyramidal neurons. Both MK-801 and CNQX blocked the pyramidal cell death in CA3 hippocampal region induced by KA. In the immunocytochemical study, KA dramatically increased the phosphorylated ERK (p-ERK) and decreased the phosphorylated CREB (p-CREB) in the hippocmapus. Both MK-801 and CNQX attenuated, in part, the increased p-ERK and the decreased p-CREB induced by KA. In addition, both MK-801 and CNQX partially reduced the increased c-Fos and c-Jun protein expression in hippocampus induced by KA. Our results suggest that both NMDA and non-NMDA receptors are involved in supraspinally administered KA-induced pyramidal cell death in CA3 region of hippocampus in the mouse and the p-ERK and the dephosphorylation of CREB protein may play an important role in CA3 region cell death of the hippocampus induced by KA administered supraspinally. Furthermore, c-Fos and c-Jun proteins may serve as third messengers responsible for CA3 pyramidal cell death induced by supraspinally administered KA.

Authors+Show Affiliations

Department of Pharmacology and Institute of Natural Medicine, College of Medicine, Hallym University, Chunchon 200-702, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12521295

Citation

Lee, Jin-Koo, et al. "Effects of MK-801 and CNQX On Various Neurotoxic Responses Induced By Kainic Acid in Mice." Molecules and Cells, vol. 14, no. 3, 2002, pp. 339-47.
Lee JK, Choi SS, Lee HK, et al. Effects of MK-801 and CNQX on various neurotoxic responses induced by kainic acid in mice. Mol Cells. 2002;14(3):339-47.
Lee, J. K., Choi, S. S., Lee, H. K., Han, K. J., Han, E. J., & Suh, H. W. (2002). Effects of MK-801 and CNQX on various neurotoxic responses induced by kainic acid in mice. Molecules and Cells, 14(3), 339-47.
Lee JK, et al. Effects of MK-801 and CNQX On Various Neurotoxic Responses Induced By Kainic Acid in Mice. Mol Cells. 2002 Dec 31;14(3):339-47. PubMed PMID: 12521295.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of MK-801 and CNQX on various neurotoxic responses induced by kainic acid in mice. AU - Lee,Jin-Koo, AU - Choi,Seong-Soo, AU - Lee,Han-Kyu, AU - Han,Ki-Jung, AU - Han,Eun-Jung, AU - Suh,Hong-Won, PY - 2003/1/11/pubmed PY - 2003/6/14/medline PY - 2003/1/11/entrez SP - 339 EP - 47 JF - Molecules and cells JO - Mol Cells VL - 14 IS - 3 N2 - Effects of MK-801 (a NMDA receptor blocker) and CNQX (6-cyano-7-nitroquinoxaline-2,3-dione; a non-NMDA receptor blocker) on several neurotoxic responses induced by kainic acid (KA) were examined in ICR mice. In a lethality test, intracerebroventricular (i.c.v.) pretreatment of MK-801 (1 microg), but not CNQX (0.5 microg), attenuated the time to lethality induced by KA (0.5 microg) administered i.c.v. In the memory test (a passive avoidance test), MK-801, but not CNQX, prevented the memory loss induced by KA (0.1 microg). The damage induced by KA (0.1 microg) administered i.c.v. in the hippocampus was markedly concentrated in the CA3 pyramidal neurons. Both MK-801 and CNQX blocked the pyramidal cell death in CA3 hippocampal region induced by KA. In the immunocytochemical study, KA dramatically increased the phosphorylated ERK (p-ERK) and decreased the phosphorylated CREB (p-CREB) in the hippocmapus. Both MK-801 and CNQX attenuated, in part, the increased p-ERK and the decreased p-CREB induced by KA. In addition, both MK-801 and CNQX partially reduced the increased c-Fos and c-Jun protein expression in hippocampus induced by KA. Our results suggest that both NMDA and non-NMDA receptors are involved in supraspinally administered KA-induced pyramidal cell death in CA3 region of hippocampus in the mouse and the p-ERK and the dephosphorylation of CREB protein may play an important role in CA3 region cell death of the hippocampus induced by KA administered supraspinally. Furthermore, c-Fos and c-Jun proteins may serve as third messengers responsible for CA3 pyramidal cell death induced by supraspinally administered KA. SN - 1016-8478 UR - https://www.unboundmedicine.com/medline/citation/12521295/Effects_of_MK_801_and_CNQX_on_various_neurotoxic_responses_induced_by_kainic_acid_in_mice_ L2 - http://www.molcells.org/journal/view.html?year=2002&volume=14&number=3&spage=339 DB - PRIME DP - Unbound Medicine ER -