Prolonged expression of c-Fos and c-Jun in the cerebral cortex of rats after deltamethrin treatment.

In this study we investigated the effects of deltamethrin on the expression of c-Fos and c-Jun in the cerebral cortex of rats. Immunohistochemical analysis demonstrated that the immunoreactivity for c-Fos was markedly increased in the cerebral cortex 5 h after deltamethrin treatment, and maintained at an increased level at 24 h, even though little immunoreactivity for c-Fos was seen in the same brain region of control rats. The immunostaining for c-Jun was also dramatically elevated in the same brain region, showing the same time course of c-Fos expression after deltamethrin treatment. Further, both MK-801, an N-methyl-D-aspartate (NMDA) receptor antagonist, and NBQX, an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)/kainate (KA) receptor antagonist, attenuated deltamethrin-elicited prolonged expression of c-Fos and c-Jun. Since the persistent expression of c-Fos and c-Jun is unusual, and has been reported before in conditions involving neurodegeneration, our results are consistent with a model that deltamethrin induces neurodegeneration through a glutamate-dependent pathway.