Increased expression of cyclin D1 in the adult rat brain following kainic acid treatment.
Recent evidence has implicated aberrant cell cycle regulation as a possible mechanism of apoptosis in non-dividing cells. We previously demonstrated increased expression of the p53 tumor suppressor gene, a prominent cell cycle regulator, in apoptotic neurons. Here we investigated the potential involvement of cyclin D1, a G1 phase cell cycle protein under p53 regulation, in kainic acid-mediated neuronal degeneration. Adult male Sprague-Dawley rats were treated systemically with kainic acid and sacrificed between 1 h and 5 days following seizure onset. Cyclin D1 expression was studied by Western blot analysis and immunohistochemistry using a rabbit polyclonal anti-cyclin D1 antibody. In untreated control rats low levels of cyclin D1 expression were detected in multiple brain regions. Between 8 and 16 h after the onset of kainic acid-induced seizures, increased cyclin D1 immunoreactivity was observed in vulnerable hippocampal pyramidal cells. Five days after seizure onset increased cyclin D1 expression was evident in reactive astrocytes. These results support a role for cyclin D1 in certain neuronal death pathways, and suggest that cyclin D1 has multiple and cell type-specific functions in the central nervous system.
Liu
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Neuroscience Program, University of Southern California, Los Angeles 90089-0191, USA.
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Tocco
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Baudry
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Schreiber
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D000818:Animals; D001921:Brain / Q000187:drug effects; D019938:Cyclin D1; D016213:Cyclins / Q000378:metabolism*; D006624:Hippocampus / Q000187:drug effects*; D007150:Immunohistochemistry; D007608:Kainic Acid / Q000494:pharmacology*; D008297:Male; D015513:Oncogene Proteins / Q000378:metabolism*; D011817:Rabbits; D051381:Rats; D017207:Rats, Sprague-Dawley
D016213:Cyclins; D015513:Oncogene Proteins; D019938:Cyclin D1; D007608:Kainic Acid