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USING in situhybridization histochemistry and immunocytochemistry the induction of immediate early genes (IEGs) was studied in the rat superior cervical ganglion (SCG) after deafferentation, axotomy and sialectomy (removal of the submandibular gland). Control SCGs showed very low levels of IEGs, whereby Fos proteins were found in 1 and Jun protein in 6 of neurons, but not in non-neuronal cells. Denervation and axotomy induced C-fos, NGFI-A, c-jun, junB and junD mRNA expression for up to 6 days in non-neuronal cells, whereas in sympathetic neurons the expression of only c-junmRNA was induced after axotomy and sialectomy. The induction of Fos and Jun proteins by neuronal injury was demonstrated by immunocytochemistry. The results indicate that neuronal injury induces IEGs mainly in non-neuronal cells and that in neurons only c-junis induced after axotomy. It is hypothesized that the induction of IEG other than c-junin neurons after brain injury is an indirect event unrelated to the neuronal response to injury.

THIS paper describes the localization of the a-type peroxisome proliferator-activated receptor (PPARa) in the rat brain using immunocytochemistry and in situhybridization. Expression of PPARa mRNA was highest in the granular cells of the cerebellar cortex and in the dentate gyrus, with a somewhat lower expresssion in areas CA1-CA4 of the hippocampus. PPARa mRNA was also found in some neurones of the cerebral cortex (layers II-IV) and the molecular layer of the cerebellar cortex, and in the olfactory tubercle. Immunocytochemistry revealed nuclear PPARα-immunoreactivity (-IR) in the same areas as seen with the in situhybridization. Furthermore, PPARa-IR was also localized in oligodendrocytes, whereas the other glial cell types appeared to lack PPARα. These results suggest that peroxisome proliferators and chemicals acting similarly have effects on discrete populations of neurones. The presence of PPARa in oligodendrocytes lends further support to the suggestion that peroxisomes are imprortant in the assembly and degradation of myelin.