Kainic acid-induced neuronal loss and glial changes in the hippocampal CA3 of p53-deficient mouse

被引:10
作者
Kitamura, Y
Ota, T
Matsuoka, Y
Okazaki, M
Kakimura, J
Tooyama, I
Kimura, H
Shimohama, S
Gebicke-Haerter, PJ
Nomura, Y
Taniguchi, T [1 ]
机构
[1] Kyoto Pharmaceut Univ, Dept Neurobiol, Kyoto 6078412, Japan
[2] Shiga Univ Med Sci, Inst Mol Neurobiol, Div Neurochem, Otsu, Shiga 5202192, Japan
[3] Shiga Univ Med Sci, Inst Mol Neurobiol, Div Neuroanat, Otsu, Shiga 5202192, Japan
[4] Kyoto Univ, Fac Med, Dept Neurol, Kyoto 6068507, Japan
[5] Univ Freiburg, Dept Psychiat & Psychotherapy, D-79104 Freiburg, Germany
[6] Hokkaido Univ, Fac Pharmaceut Sci, Dept Pharmacol, Sapporo, Hokkaido 0600812, Japan
关键词
p53-deficient mouse; kainic acid; phosphorylated c-Jun; neuronal loss; microglia; astrocytes; hippocampal CA3;
D O I
10.1016/S0304-3940(98)00714-9
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
We examined kainic acid (KA)-induced neuronal death and changes in glial cells in p53-deficient (p53(-/-)) and wild-type (p53(+/+)) mice which were CBA and C57BL/6 background. The p53(-/-) mouse exhibited a KA-induced loss of CA3 pyramidal neurons similar to that in wild-type mouse. Before neuronal death, c-Jun protein was expressed, phosphorylated and translocated into several nuclei of CA3 pyramidal neurons. In p53(-/-) mouse, microglial activation was slightly faster and more continuous after 1-7 days than that in p53(+/+) mouse. On the other hand, p53(-/-) astrocytes were relatively resistant to KA cytotoxicity, and marked astrocytosis also occurred after 7 days. These observations suggest that p53-null mutation may influence the activation and proliferation of glial cells rather than neuronal death. (C) 1998 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:57 / 60
页数:4
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