Neuroendocrine regulation of broodiness in the domestic hen

Abstract

Broodiness in the domestic hen is characterized by incubation of eggs and subsequent care of the young. Incubation behaviour is initiated by increased plasma progesterone and oestrogen from maturing ovarian follicles that induce nesting behaviour. This is subsequently transformed into incubation behaviour by increased plasma prolactin in association with decreased gonadotrophin and ovarian steroid secretion. Gonadotrophin secretion is under the stimulatory and inhibitory control, respectively, of gonadotrophin releasing hormone-I (GnRFI-I) and gonadotrophin inhibitory hormone (GnIH).
Prolactin secretion is controlled by the stimulatory action of the hypothalamic neuropeptide, vasoactive intestinal polypeptide (VIP). The aim of this study was to increase understanding and knowledge of the interactions between these hormones and neuropeptide in the neuroendocrine control of incubation behaviour in the domestic hen. Observations were made using fluorescence immunocytochemistry with additional data on progesterone receptor mRNAs, using PCR to localize the receptor.
Hypothalamic progesterone receptor immunoreactivity (PR-ir) was seen in several hypothalamic nuclei and areas including the organum vasculoswn terminalis (OVLT) and basal hypothalamic tuberal region (TU). The density of cells containing PR-ir in the OVLT and TU, but not at other hypothalamic loci, was lower in incubating than in laying hens. In the anterior pituitary gland, PR-ir was localised in luteinizing hormone (LH) but not prolactin cells, and the density of cells containing LH and PR-ir was lower in incubating than in laying hens. The density of prolactin cells was higher in incubating than in laying hens. Progesterone receptor B mRNA was found in It the TU and pituitary gland in both laying and incubating hens. Prolactin
receptor, but not progesterone receptor, was co-localised in VIP neurones in the TU. The number of visible VIP-ir cell bodies containing prolactin receptor was greater in incubating than in laying hens. Nerve fibres containing VIP did not contact GnRH-I-ir cell bodies, but potential contact between those VIP and GnRJ-I-I fibres was seen in the median eminence. GnIH was localized in cells in the paraventricular nucleus (PVN) in incubating and laying hens did not contain PR-ir and had terminals in the median eminence. The density of GnIH neurones did not differ between laying and incubating hens, but their size of the cell bodies was significantly larger in incubating hens. Although GnRFI-Iir and GnIH-ir fibres were abundant in the PVN, they were not observed to come into close contact.
It is concluded that incubation behaviour and associated changes in either prolactin or gonadotrophin secretion could be mediated through progesterone receptor B in the OVLT and TU. Progesterone is likely to exert feed-back control of LH secretion at the level of the pituitary gland in laying, but not in incubating hens through progesterone receptor B. Prolactin may act directly on basal hypothalamic VIP neurones to regulate it own secretion. Increased GnIH release in incubating hens may contribute to depressed gonadotrophin secretion.