Beltramo M, Calas A, Chernigovskaya E, Thibault J, Ugrumov M
Département de Neurobiologie des Signaux Intercellulaires, Institut des Neurosciences, CNRS URA 1488, Université P. et M. Curie, Paris, France.
Neuroscience. 1997 Jul;79(2):555-61. doi: 10.1016/s0306-4522(96)00694-x.
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.
根据我们早期的研究，新生大鼠体内儿茶酚胺的消耗会刺激视上核神经元中血管加压素和催产素基因的表达。本研究拓展了这一方向，评估儿茶酚胺缺乏是否对视上核中正在分化的血管加压素和催产素神经元产生长期影响。首先，从妊娠第9天至第21天，每天给怀孕大鼠注射儿茶酚胺合成抑制剂α-甲基对酪氨酸，然后从出生后第2天至第10天给它们的幼崽注射该抑制剂，以使儿茶酚胺消耗。注射生理盐水而非药物的动物作为对照。将经过药物处理的大鼠和对照大鼠在正常实验室条件下饲养四个月，然后分别对其进行材料处理，用于血管加压素和催产素信使核糖核酸及肽的半定量原位杂交和免疫细胞化学分析。与对照组相比，预先进行儿茶酚胺消耗的大鼠视上核中血管加压素和催产素信使核糖核酸浓度没有差异。相反，儿茶酚胺缺乏导致细胞体和突起中血管加压素免疫反应性物质的含量增加。催产素免疫反应性细胞体也出现这种情况，但仅在雌性大鼠中出现，这表明儿茶酚胺在其作用中与性类固醇存在相互干扰。与对照组相比，经过药物处理的大鼠中血管加压素和催产素神经元的数量和大小没有变化。因此，在神经元分化过程中儿茶酚胺缺乏导致血管加压素和催产素细胞内含量长期增加，但不影响血管加压素和催产素基因的表达。这可能更多地是由肽释放水平降低而非肽产生水平增加来解释。
