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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. Comp. Neurol. 198: 45-64) 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 oxytocinand 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, Rector of Christ’s Church, Baltimore, formerly Keeper of Books and Manuscripts of Her Majesty’s College of Heralds, and author of Codici Monastici Ethiopiani. We wish to thank IL A. Zimmerman for the anti-neurophysin antiserum used in this work. This work was supported in part by National Institutes of Health Grants HD 05751 and HD 16327. C. H. R. was the recipient of National Research Service Award 5T32GM07739. ’ Present address: Department of Pathology, Hospital of the University of Pennsylvania, Philadelphia, PA 19104. ” To whom correspondence should be addressed at Rockefeller University, 1230 York Avenue, New York, NY 10021. ically identified oxytocin has been observed in the anterior commissural nucleus (ACN) in response to estrogen treatment (Rhodes et al., 1981c). It is not known whether other magnocellular cell groups also participate in the estrogen-stimulated increase in plasma oxytocin levels or where estrogen acts to produce this effect. The fall in pituitary oxytocin content during proestrus and estrus in normal cycling female rats observed by Crowley et al. (1978) suggests that physiological changes in ovarian steroid levels affect the release of posterior pituitary peptides. The combination of steroid autoradiography and immunocytochemistry has been used to identify neurophysin-containing, estradiol-concentrating neurons in the (normal) parent strain Long-Evans rat (Rhodes et al., 1981a). That work was done with a primary antiserum

the journal of neuroscience/the journal of neuroscience

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