Kainate, a potent excitatory and neurotoxic agent, has also proved useful in studies on other glutamate‐driven phenomena, such as neuronal plasticity. Long‐term effects of kainate are apparently dependent on its influence on the expression of various genes, including those encoding the AP‐1 transcription factor, consisting of proteins belonging to the Fos and Jun families. In our studies we analysed c‐fos, fos B, c‐jun, jun B and jun D mRNA levels as well as a functional feature of AP‐1, its DNA‐binding activity, in the rat brain following systemic injection of kainate. Two phases of elevated AP‐1 DNA‐binding activity were observed in the hippocampus and entorhinal cortex, and were correlated with period of seizures (2 and 6 h after kainate injection) and neuron damage (48–72 h). At 72 h after kainate treatment DNA fragmentation, believed to be diagnostic of apoptotic processes typical of programmed cell death phenomena, was noted. Two and six hours after the treatment, AP‐1 consisted predominantly of Fos B, c‐Fos, Fra‐2 and Jun B, while at 72 h Jun D constituted the major AP‐1 component in place of Jun B, and no c‐Fos was detected. Only a slight AP‐1 increase was seen 24 h after kainate treatment. In the sensory cortex, only the late phase of AP‐1 elevation was detected. Contrary to AP‐1, no effect of kainate on levels of two other transcription factors, CREB/ATF (cAMP‐responsive element binding proteins) and OCT (octamer element DNA‐binding activity) was seen. However, the level of OCT DNA‐binding activity was higher in the sensory cortex than in other two structures examined. These data point to a selective effect of kainate on AP‐1 in brain structures known to be particularly vulnerable to kainate, and suggest a role of AP‐1 transcription factor, and more selectively Jun D protein, in kainate‐driven programmed neuronal death.
European Journal of Neuroscience – Wiley
Published: Oct 1, 1994
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