title: Long-lasting effect of catecholamine deficiency on differentiating vasopressin and oxytocin neurons in the rat supraoptic nucleus.
abstract: According to our earlier study, the catecholamine depletion in neonatal rats resulted in stimulation of the vasopressin and oxytocin gene expression in the neurons of the supraoptic nucleus. The present study 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 depleted 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 10th postnatal day. The animals, injected with saline instead of drugs, served as controls. The pharmacologically-treated and control rats were kept for four months under normal laboratory conditions until processing the materials for semi-quantitative in situ hybridization and immunocytochemistry of vasopressin and oxytocin messenger RNAs and peptides, respectively. There were no differences in the vasopressin and oxytocin messenger RNA concentrations in the supraoptic nucleus in rats following preliminary catecholamine depletion compared to controls. Conversely, the catecholamine deficiency resulted in an increased content of the vasopressin-immunoreactive material in cell bodies and processes. 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 and oxytocin neurons did not change in pharmacologically-treated rats compared to the controls. Thus, the catecholamine deficiency in the course of the neuron differentiation resulted in a long-lasting augmentation of the intracellular content of vasopressin and oxytocin but did not 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.
authors.affiliation: Département de Neurobiologie des Signaux Intercellulaires, Institut des Neurosciences, CNRS URA 1488, Université P. et M. Curie, Paris, France.
authors.forename: M
authors.initials: M
authors.lastname: Beltramo
authors.forename: A
authors.initials: A
authors.lastname: Calas
authors.forename: E
authors.initials: E
authors.lastname: Chernigovskaya
authors.forename: J
authors.initials: J
authors.lastname: Thibault
authors.forename: M
authors.initials: M
authors.lastname: Ugrumov
mesh_terms: D000818:Animals; D002395:Catecholamines / Q000172:deficiency*; D005260:Female; D017403:In Situ Hybridization; D009474:Neurons / Q000378:metabolism*; D010121:Oxytocin / Q000378:metabolism*; D011247:Pregnancy; D051381:Rats; D017208:Rats, Wistar; D013495:Supraoptic Nucleus / Q000378:metabolism*; D013997:Time Factors; D014667:Vasopressins / Q000378:metabolism*
chemical_list: D002395:Catecholamines; D014667:Vasopressins; D010121:Oxytocin