No abstract

An increase in neuronal glutamate transporter expression after nerve injury was demonstrated by means of differential display PCR (DD-PCR) coupled with in situ hybridization. DD-PCR was carried out to compare differences in expression of mRNAs between axotomized and normal hypoglossal motoneurons in the rat. The expression of several gene fragments were found to be increased following nerve injury; the full length cDNA corresponding to one fragment was cloned by subsequent rat cDNA library screening. The close homology of glutamate transporters with our rat cDNA led us to conclude that this clone corresponds to the rat neuronal glutamate transporter (rat EAAC1). We speculate that the upregulation of this glutamate uptake system may increase the resistance of these cells against neurotoxic glutamate accumulation during the process of nerve regeneration.

An increase in cyclin G expression after nerve injury was demonstrated by differential display PCR, carried out to compare references in expression of mRNAs between axotomized and normal hypoglossal motoneurons in the rat. The nerve injury dramatically upregulated the expression of cyclin G mRNA in the motoneurons during the early phase of the nerve regeneration process, suggesting an involvement of cyclin G in the early stage of nerve regeneration. In brain, in situ hybridization studies also demonstrated cyclin G expression in a restricted group of matured neurons, particularly in the telencephalon and the thalamus. This constitutive expression in mature neurons suggests that cyclin G may have a function different from other members of the cyclin group. In addition, although cyclin G has been shown to be a transcription target of p53, the upregulation of cyclin G in injured motoneurons, as well as the expression in the adult rat brain, was not affected in the p53-deficient mouse. These data suggest that the expression of cyclin G, at least in the nervous system, is not regulated by p53 predominantly, and that there may be alternative regulatory factors or pathways for cyclin G expression.

No abstract

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