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Role of nicotinic acetylcholine receptors in the regulation of kainic acid-induced hippocampal cell death in mice.
Brain Res Bull. 2004 Dec 15; 64(4):309-17.BR

Abstract

Kainic acid (KA) is a well-known excitatory, neurotoxic substance. In mice, morphological damage of hippocampus induced by KA administered intracerebroventricularly (i.c.v.) was markedly concentrated on the CA3 pyramidal neurons. In the present study, the possible role of nicotinic acetylcholine receptors (nAchRs) in hippocampal cell death induced by KA (0.1 microg) administered i.c.v. was examined. Methyllycaconitine (MC; nAchRs antagonist, 20 microg) attenuated KA-induced CA3 pyramidal cell death. KA increased immunoreactivities (IRs) of phorylated extracellular signal-regulated kinase (p-ERK; at 30 min), p-CaMK II (at 30 min), c-Fos (at 2 h), c-Jun (at 2 h), glial fibrillary acidic protein (GFAP at 1 day), and the complement receptor type 3 (OX-42; at 1 day) in hippocampal area. MC attenuated selectively KA-induced p-CaMK II, GFAP and OX-42 IR in the hippocampal CA3 region. Our results suggest that p-CaMK II may play as an important regulator responsible for the hippocampal cell death induced by KA administered i.c.v. in mice. Reactive astrocytes, which was meant by GFAP IR, and activated microglia, which was meant by OX-42 IR, may be a good indicator for measuring the cell death in hippocampal regions by KA-induced excitotoxicity. Furthermore, it is implicated that niconitic 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, 1 Okchun-Dong, Chunchon, Kangwon-Do 200-702, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15561465

Citation

Lee, Han-Kyu, et al. "Role of Nicotinic Acetylcholine Receptors in the Regulation of Kainic Acid-induced Hippocampal Cell Death in Mice." Brain Research Bulletin, vol. 64, no. 4, 2004, pp. 309-17.
Lee HK, Choi SS, Han EJ, et al. Role of nicotinic acetylcholine receptors in the regulation of kainic acid-induced hippocampal cell death in mice. Brain Res Bull. 2004;64(4):309-17.
Lee, H. K., Choi, S. S., Han, E. J., Lee, J. Y., Kwon, M. S., Shim, E. J., Seo, Y. J., & Suh, H. W. (2004). Role of nicotinic acetylcholine receptors in the regulation of kainic acid-induced hippocampal cell death in mice. Brain Research Bulletin, 64(4), 309-17.
Lee HK, et al. Role of Nicotinic Acetylcholine Receptors in the Regulation of Kainic Acid-induced Hippocampal Cell Death in Mice. Brain Res Bull. 2004 Dec 15;64(4):309-17. PubMed PMID: 15561465.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Role of nicotinic acetylcholine receptors in the regulation of kainic acid-induced hippocampal cell death in mice. AU - Lee,Han-Kyu, AU - Choi,Seong-Soo, AU - Han,Eun-Jung, AU - Lee,Jin-Young, AU - Kwon,Min-Soo, AU - Shim,Eon-Jeong, AU - Seo,Young-Jun, AU - Suh,Hong-Won, PY - 2004/03/15/received PY - 2004/07/05/revised PY - 2004/08/06/accepted PY - 2004/11/25/pubmed PY - 2005/3/15/medline PY - 2004/11/25/entrez SP - 309 EP - 17 JF - Brain research bulletin JO - Brain Res Bull VL - 64 IS - 4 N2 - Kainic acid (KA) is a well-known excitatory, neurotoxic substance. In mice, morphological damage of hippocampus induced by KA administered intracerebroventricularly (i.c.v.) was markedly concentrated on the CA3 pyramidal neurons. In the present study, the possible role of nicotinic acetylcholine receptors (nAchRs) in hippocampal cell death induced by KA (0.1 microg) administered i.c.v. was examined. Methyllycaconitine (MC; nAchRs antagonist, 20 microg) attenuated KA-induced CA3 pyramidal cell death. KA increased immunoreactivities (IRs) of phorylated extracellular signal-regulated kinase (p-ERK; at 30 min), p-CaMK II (at 30 min), c-Fos (at 2 h), c-Jun (at 2 h), glial fibrillary acidic protein (GFAP at 1 day), and the complement receptor type 3 (OX-42; at 1 day) in hippocampal area. MC attenuated selectively KA-induced p-CaMK II, GFAP and OX-42 IR in the hippocampal CA3 region. Our results suggest that p-CaMK II may play as an important regulator responsible for the hippocampal cell death induced by KA administered i.c.v. in mice. Reactive astrocytes, which was meant by GFAP IR, and activated microglia, which was meant by OX-42 IR, may be a good indicator for measuring the cell death in hippocampal regions by KA-induced excitotoxicity. Furthermore, it is implicated that niconitic receptors appear to be involved in hippocampal CA3 pyramidal cell death induced by KA administered i.c.v. in mice. SN - 0361-9230 UR - https://www.unboundmedicine.com/medline/citation/15561465/Role_of_nicotinic_acetylcholine_receptors_in_the_regulation_of_kainic_acid_induced_hippocampal_cell_death_in_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0361-9230(04)00208-4 DB - PRIME DP - Unbound Medicine ER -