Estrogen-concentrating neurophysin-containing hypothalamic magnocellular neurons in the vasopressin-deficient (Brattleboro) rat: a study combining steroid autoradiography and immunocytochemistry

Abstract

This report describes the distribution of neurophysin-containing, estradiol-concentrating neurons in a strain of rat which is congenitally unable to produce vasopressin and its associated neurophysin (the Brattleboro rat). In this strain of rat, all of the neurophysin-containing cells are oxytocin producing. The magnocellular neurons which produce vasopressin in the normal rat are present in their normal numbers and normal locations (Rhodes, C. H., J. I. Morrell, and D. W. Pfaff (1981) J. ) and can be identified as the neurophysin-negative magnocellular neurons.Estradiol-concentrating cell nuclei were observed in magnocellular neurons with neurophysincontaining cytoplasm as well as in magnocellular neurons lacking immunocytochemically detectable neurophysin. The majority of these neurons were found in the paraventricular nucleus (PVN), ventral and medial to its lateral subnucleus, and in the posterior subnucleus of the PVN. There were, in addition, many neurophysin-containing and neurophysin-lacking magnocellular neurons with nuclei which did not concentrate estradiol. Within the PVN, the majority of the neurophysinnegative, non-estradiol-concentrating neurons were in the lateral subnucleus, while the majority of the neurophysin-positive, non-estradiol-concentrating neurons were in the medial subnucleus.Comparison of the results of experiments using homozygous Brattleboro rats with the results of similar experiments using the (normal) parent strain Long-Evans rat suggests that, in the normal animals, there are both oxytocin-and vasopressin-producing neurons which concentrate estradiol. Comparison of these observations with published descriptions of the anatomical distribution of neurons which project to the medulla or spinal cord suggests that many of the oxytocin-.or vasopressin-containing, estrogen-concentrating neurons in the PVN send axons to regions regulating autonomic functions.Estrogen treatment is a stimulus for the release of oxytocin (Yamaguchi et al., 1979) and vasopressin (Skowsky et al., 1979). A decrease in immunocytochem-' This paper is dedicated to the Rev. Dr. Winthrop Brainerd,

An alternate pathway for androgen regulation of brain function: Activation of estrogen receptor beta by the metabolite of dihydrotestosterone, 5α-androstane-3β,17β-diol

“…In the PVN there was some 3 H-estradioluptake into magnocellular regions, although the amounts were small compared to periventricular and preoptic areas. 3 H-estradiol-uptake was also demonstrated in arginine vasopressin (AVP) containing magnocellular neurons (Rhodes et al, 1982). Although for years sensitivity (and in retrospect, specificity) was the limiting factor with such approaches, the recent development of high specific activity ligands demonstrated robust estradiol-uptake by PVN neurons .…”

Pituitary Portal Plasma Levels of Oxytocin during the Estrous Cycle, Lactation, and Hyperprolactinemia

“…[49][50][51][52][53][54][55][56][57] Furthermore, recent studies have provided evidence of a gonadal steroid modulatory role on OT synthesis in the hypothalamus and of gonadal steroid induction of OT receptors in the anterior pituitary (see chapters by Brooks, Johnson, Pfaff et al, and Schumacher et al). 13 An important consideration is whether or not the OT secretory activity in the median eminence alters with the dynamic changes of the plasma level of gonadal steroids during the reproductive cycle.…”

Regulation of neuronal oxytocin mRNA by ovarian steroids in the mature and developing hypothalamus.

“…Estrogen treatment stimulates the release of oxytocin into the peripheral circulation (7), induces oxytocin binding sites in the brain (8), influences the electrical activity ofoxytocinergic neurons (9), and alters the pattern of oxytocinergic cells and fibers in the brain, as detected by immunocytochemistry (10-12). How estrogen mediates these changes is unknown, although a subpopulation of oxytocinergic neurons have binding sites for estradiol (13,14).We are interested in neural correlates of behavioral changes that accompany puberty. To determine whether the oxytocinergic system is modified by increased ovarian steroids during female adolescence, we have investigated neuronal levels of oxytocin mRNA before, during, and after puberty using Northern blot and in situ hybridization analyses.…”