Long-term modulation by postnatal oxytocin of the α2-adrenoceptor agonist binding sites in central autonomic regions and the role of prenatal stress
2004 (English)In: Journal of neuroendocrinology (Print), ISSN 0953-8194, E-ISSN 1365-2826, Vol. 16, no 3, 183-190 p.Article in journal (Refereed) Published
The aim of this work was to evaluate whether oxytocin administered in male rats subcutaneously early in life in the absence or presence of food restriction during pregnancy has life-long effects on the α2-agonist binding sites in the nucleus of the solitarii tract (NTS), in the hypothalamus and the amygdala, as evaluated by quantitative receptor autoradiography. Maternal food restriction alone increased the affinity of the α2-agonist [3H]UK14.304 binding sites exclusively in the NTS. In offspring from ad libitum fed dams, oxytocin treatment significantly increased the density of α2-agonist binding sites in the NTS and in the hypothalamus. The Kd value of the α2-agonist binding sites in the hypothalamus of these rats, but not in the other regions studied, was also significantly increased. In offspring from food-restricted dams, oxytocin treatment produced a significant increase of the Bmax values in the hypothalamus and the amygdala and the Kd value of the α2-agonist binding sites in the NTS of these rats also was selectively and significantly increased. These results suggest that a postnatal, oxytocin-induced increase of regional α2-adrenoceptor function can be seen in adulthood by a persistent, regionally selective increase in the density of central α2-adrenoceptor agonist binding sites, in the absence of an affinity change in the NTS. Such a regional increase of α2-adrenoceptor signalling in adulthood may contribute to the anti-stress action of postnatal oxytocin. By contrast, after prenatal stress, the potential increase in α2-adrenoceptor signalling takes place via selective increases of density with no changes of affinity of the α2-agonist binding sites in the hypothalamus and the amygdala.
Place, publisher, year, edition, pages
2004. Vol. 16, no 3, 183-190 p.
Medical and Health Sciences
IdentifiersURN: urn:nbn:se:liu:diva-23586DOI: 10.1111/j.0953-8194.2004.01146.xLocal ID: 3072OAI: oai:DiVA.org:liu-23586DiVA: diva2:243901