LONG-LASTING EFFECT OF CATECHOLAMINE DEFICIENCY ON DIFFERENTIATING VASOPRESSIN AND OXYTOCIN NEURONS IN THE RAT SUPRAOPTIC NUCLEUS

According to our earlier study, the catecholamine depletion in neonata l rats resulted in stimulation of the vasopressin and oxytocin gene ex pression in the neurons of the supraoptic nucleus.(30) The present stu dy extends this line, evaluating whether the catecholamine deficiency provides a long-lasting effect on the differentiating vasopressin and oxytocin neurons of the supraoptic nucleus. Catecholamines were deplet ed by daily injections of an inhibitor of the catecholamine synthesis, alpha-methyl-p-tyrosine, first, to pregnant rats From the 9th to the 21st day of gestation and, then, to their pups from the 2nd to the 10t h postnatal day. The animals, injected with saline instead of drugs, s erved as controls. The pharmacologically-treated and control rats were kept for four months under normal laboratory conditions until process ing the materials for semi-quantitative in situ hybridization and immu nocytochemistry of vasopressin and oxytocin messenger RNAs and peptide s, respectively. There were no differences in the vasopressin and oxyt ocin messenger RNA concentrations in the supraoptic nucleus in rats fo llowing preliminary catecholamine depletion compared to controls. Conv ersely, the catecholamine deficiency resulted in an increased content of the vasopressin-immunoreactive material in cell bodies and processe s. This was also the case for the oxytocin-immunoreactive cell bodies but only in females, suggesting an interference of catecholamines with sexual steroids in their action. The number and size of vasopressin a nd oxytocin neurons did not change in pharmacologically-treated rats c ompared to the controls. Thus, the catecholamine deficiency in the cou rse of the neuron differentiation resulted in a long-lasting augmentat ion of the intracellular content of vasopressin and oxytocin but did n ot influence the vasopressin and oxytocin gene expression. This might be explained rather by the reduced level of peptide release than by an increased level of the peptide production. (C) 1997 IBRO.