In primary culture, type I astroglial cells from neocortex of newborn rats express the proenkephalin gene. The glial cells are not homogeneous but differ in their morphology; i.e., polygonal and process-bearing cells are found. Transcription of the proenkephalin gene is increased via protein kinase A upon stimulation with cyclic AMP (cAMP) analogues. In the present study, how noradrenaline affected the expression of the proenkephalin gene in both cell types was investigated. Noradrenaline enhanced the levels of proenkephalin mRNA in a concentration-dependent manner. Experiments with subtypeselective antagonists suggested that /91-adrenoceptors were involved. In situ hybridization showed that proenkephalin mRNA was induced only in polygonal cells. Noradrenaline also increased the levels of cAMP. However, concentrations of noradrenaline that produced a maximal increase in cAMP caused only submaximal elevations of proenkephalin mRNA. This discrepancy was explained by the finding that noradrenaline increased the expression of the proenkephalin gene also via a1-adrenoceptors. It is concluded that i3~-and a1-adrenoceptors can act in a synergistic manner on the expression of the proenkepha in gene in astroglial cells.
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