Effect of neonatal 6-hydroxydopamine treatment on alpha 1- and alpha 2-adrenoceptors in rat cerebral cortex.

Neonatal 6-hydroxydopamine (6-OHDA) treatment was used to destroy the noradrenergic nerve endings in rat cerebral cortex and thus give some insight into the development and regulation of alpha-adrenoceptor subtypes, which in turn provides information concerning the anatomical localization of alpha 1- and alpha 2-adrenoceptors. In cerebral cortex of rats treated in the neonatal period with 6-OHDA, we have observed an irreversible decrease in noradrenaline levels. Differences in 3H-clonidine and 3H-prazosin binding occurred which varied depending upon the time between denervation and the binding assay. In 7-14 day-old rats we observed a 20% decrease in the number of alpha 2-adrenoceptors and a marked increase in alpha 1-adrenoceptors. In older rats (45-50 day-old) both types of alpha-adrenoceptors were increased. Results of this study indicate that alpha 2-adrenoceptors located on presynaptic noradrenergic terminals represent only a minor fraction of the total alpha 2- adrenoceptors in rat cerebral cortex that are lost after denervation. Conversely, noradrenergic denervation resulted in supersensitivity of the alpha 1-adrenoceptors and nonnoradrenergic terminals located on alpha 2-adrenoceptors.