Kitamura Y, Ota T, Matsuoka Y, Okazaki M, Kakimura J, Tooyama I, Kimura H, Shimohama S, Gebicke-Haerter P J, Nomura Y, Taniguchi T
Department of Neurobiology, Kyoto Pharmaceutical University, Japan.
Neurosci Lett. 1998 Oct 9;255(1):57-60. doi: 10.1016/s0304-3940(98)00714-9.
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.
