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Role of gamma-aminobutyricacidB(GABA(B)) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus.
Exp Mol Med. 2005 Dec 31; 37(6):533-45.EM

Abstract

Kainic acid (KA) is well-known as an excitatory, neurotoxic substance. In mice, KA administered intracerebroventricularly (i.c.v.) lead to morphological damage of hippocampus expecially concentrated on the CA3 pyramidal neurons. In the present study, the possible role of gamma-aminobutyric acid B (GABA(B)) receptors in hippocampal cell death induced by KA (0.1 microg) administered i.c.v. was examined. 5-Aminovaleric acid (5-AV; GABA(B) receptors antagonist, 20 mug) reduced KA-induced CA3 pyramidal cell death. KA increased the phosphorylated extracellular signal-regulated kinase (p-ERK) and Ca(2+)/calmodulin-dependent protein kinase II (p-CaMK II) immunoreactivities (IRs) 30 min after KA treatment, and c-Fos, c-Jun IR 2 h, and glial fibrillary acidic protein (GFAP), complement receptor type 3 (OX-42) IR 1 day in hippocampal area in KA-injected mice. 5-AV attenuated KA-induced p-CaMK II, GFAP and OX-42 IR in the hippocampal CA3 region. These results suggest that p-CaMK II may play as an important regulator on hippocampal cell death induced by KA administered i.c.v. in mice. Activated astrocytes, which was presented by GFAP IR, and activated microglia, which was presented by the OX-42 IR, may be a good indicator for measuring the cell death in hippocampal regions by KA excitotoxicity. Furthermore, it showed that GABA(B) receptors appear to be involved in hippocampal CA3 pyramidal cell death induced by KA administered i.c.v. in mice.

Authors+Show Affiliations

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

16391514

Citation

Lee, Han Kyu, et al. "Role of gamma-aminobutyricacidB(GABA(B)) Receptors in the Regulation of Kainic Acid-induced Cell Death in Mouse Hippocampus." Experimental & Molecular Medicine, vol. 37, no. 6, 2005, pp. 533-45.
Lee HK, Seo YJ, Choi SS, et al. Role of gamma-aminobutyricacidB(GABA(B)) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus. Exp Mol Med. 2005;37(6):533-45.
Lee, H. K., Seo, Y. J., Choi, S. S., Kwon, M. S., Shim, E. J., Lee, J. Y., & Suh, H. W. (2005). Role of gamma-aminobutyricacidB(GABA(B)) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus. Experimental & Molecular Medicine, 37(6), 533-45.
Lee HK, et al. Role of gamma-aminobutyricacidB(GABA(B)) Receptors in the Regulation of Kainic Acid-induced Cell Death in Mouse Hippocampus. Exp Mol Med. 2005 Dec 31;37(6):533-45. PubMed PMID: 16391514.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of gamma-aminobutyricacidB(GABA(B)) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus. AU - Lee,Han Kyu, AU - Seo,Young Jun, AU - Choi,Seong Soo, AU - Kwon,Min Soo, AU - Shim,Eon Jeong, AU - Lee,Jin Young, AU - Suh,Hong Won, PY - 2006/1/5/pubmed PY - 2006/2/2/medline PY - 2006/1/5/entrez SP - 533 EP - 45 JF - Experimental & molecular medicine JO - Exp Mol Med VL - 37 IS - 6 N2 - Kainic acid (KA) is well-known as an excitatory, neurotoxic substance. In mice, KA administered intracerebroventricularly (i.c.v.) lead to morphological damage of hippocampus expecially concentrated on the CA3 pyramidal neurons. In the present study, the possible role of gamma-aminobutyric acid B (GABA(B)) receptors in hippocampal cell death induced by KA (0.1 microg) administered i.c.v. was examined. 5-Aminovaleric acid (5-AV; GABA(B) receptors antagonist, 20 mug) reduced KA-induced CA3 pyramidal cell death. KA increased the phosphorylated extracellular signal-regulated kinase (p-ERK) and Ca(2+)/calmodulin-dependent protein kinase II (p-CaMK II) immunoreactivities (IRs) 30 min after KA treatment, and c-Fos, c-Jun IR 2 h, and glial fibrillary acidic protein (GFAP), complement receptor type 3 (OX-42) IR 1 day in hippocampal area in KA-injected mice. 5-AV attenuated KA-induced p-CaMK II, GFAP and OX-42 IR in the hippocampal CA3 region. These results suggest that p-CaMK II may play as an important regulator on hippocampal cell death induced by KA administered i.c.v. in mice. Activated astrocytes, which was presented by GFAP IR, and activated microglia, which was presented by the OX-42 IR, may be a good indicator for measuring the cell death in hippocampal regions by KA excitotoxicity. Furthermore, it showed that GABA(B) receptors appear to be involved in hippocampal CA3 pyramidal cell death induced by KA administered i.c.v. in mice. SN - 1226-3613 UR - https://www.unboundmedicine.com/medline/citation/16391514/Role_of_gamma_aminobutyricacidB_GABA_B___receptors_in_the_regulation_of_kainic_acid_induced_cell_death_in_mouse_hippocampus_ L2 - https://antibodies.cancer.gov/detail/CPTC-FOS-4 DB - PRIME DP - Unbound Medicine ER -