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이한규,서영준,최성수,권민수,심은정,이진영,서홍원 생화학분자생물학회 2005 Experimental and molecular medicine Vol.37 No.6
Kainic acid (KA) is well-known as an excitatory, neurotoxic substance. In mice, KA administered intracerebroventricularly (i.c.v.) lead to morpholo-gical damage of hippocampus expecially concent-rated on the CA3 pyramidal neurons. In the present study, the possible role of γ-aminobutyric acid B (GABAB) receptors in hippocampal cell death induced by KA (0.1 g) administered i.c.v. was examined. 5-Aminovaleric acid (5-AV; GABAB recep-tors antagonist, 20 g) reduced KA-induced CA3 pyramidal cell death. KA increased the phos-phorylated extracellular signal-regulated kinase (p-ERK) and Ca2+/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 recep-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 excito-toxicity. Furthermore, it showed that GABAB recep-tors appear to be involved in hippocampal CA3 pyramidal cell death induced by KA administered i.c.v. in mice.