Sustained potentiation of AP1 DNA binding is not always associated with neuronal death following systemic administration of kainic acid in murine hippocampus
T. Kitayama et al., Sustained potentiation of AP1 DNA binding is not always associated with neuronal death following systemic administration of kainic acid in murine hippocampus, NEUROCHEM I, 35(6), 1999, pp. 453-462
Mice were intraperitoneally injected with kainic acid (KA), followed by dis
section of frozen coronal sections and subsequent punching out of the pyram
idal and granular cell layers in the hippocampus under a binocular microsco
pe. Systemic administration of KA resulted in marked and sustained potentia
tion of binding of a radiolabeled double stranded oligonucleotide probe for
the nuclear transcription factor activator protein-1 (AP1) in the pyramida
l cell layers of the CA1 and CA3 subfields and the granule cell layers of t
he dentate gyrus 2-18 h later. Morphological evaluation using cresyl violet
revealed marked losses of neuronal layers in the pyramidal CA1 and CA3 sub
fields, but not in the granular dentate gyrus, within 6 weeks after adminis
tration. Supershift analysis using antibodies against different Jun and Fos
family members differentiated between AP1 DNA binding in hippocampal nucle
ar extracts obtained 2 and 18 h after the administration of KA. These resul
ts suggest that neuronal death may not always follow modulation of de novo
synthesis of particular proteins through sustained potentiation of AP1 DNA
binding which involves expression of different Jun and Fos family members i
n response to systemic administration of KA in murine hippocampus. (C) 1999
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