PubMed · 4368026
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K Fuxe. 1971. Gonad function and tuberoinfundibular dopamine.. https://pubmed.ncbi.nlm.nih.gov/4368026/
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We provide the first evidence that prolactin is a neuromodulator of behavioral and neuroendocrine stress coping in the rat. In virgin female and male rats, intracerebral infusion of ovine prolactin (oPRL) into the lateral cerebral ventricle (intracerebroventricular) exerted an anxiolytic effect on the elevated plus-maze in a dose-dependent manner (0.1 and 1.0 microg/5 microl; p < 0.01). In contrast, downregulation of the expression of the long form of brain prolactin receptors by chronic intracerebroventricular infusion of an antisense oligodeoxynucleotide (ODN) (osmotic minipump, 0.5 microg. 0.5 microl(-1). hr(-1); 5 d) increased anxiety-related behavior on the plus-maze compared with mixed bases-treated and vehicle-treated rats (p < 0.01), again demonstrating an anxiolytic effect of PRL acting at brain level. Furthermore, in jugular vein-catheterized female rats, the stress-induced increase of corticotropin secretion was decreased after chronic intracerebroventricular infusion of oPRL (osmotic minipump, 1.0 microg. 0.5 microl(-1). hr(-1); p < 0.05) and, in contrast, was further elevated by antisense targeting of the brain prolactin receptors (p < 0.01). This provides evidence for a receptor-mediated attenuation of the responsiveness of the hypothalamo-pituitary-adrenal (HPA) axis by prolactin. The antisense ODN sequence was selected on the basis of secondary structure molecular modeling of the target mRNA to improve antisense ODN-mRNA hybridization. Receptor autoradiography confirmed the expected improvement in the efficacy of downregulation of prolactin receptor expression [empirically designed antisense, 30%; p > 0.05, not significant; adjustment of target position after mRNA modeling, 72%; p < 0.05). Taken together, prolactin acting at brain level has to be considered as a novel regulator of both emotionality and HPA axis reactivity.
Corticotropin-releasing hormone (CRH) mediates endocrine, behavioral, and autonomic responses to stress. In addition to binding to two receptor subtypes, CRH binds to a CRH-binding protein (CRH-BP). While CRH-BP is hypothesized to play a role in regulating levels of free CRH and modulating the stress response, the effects of stressors on brain CRH-BP are relatively unexplored. The present study determined effects of acute and repeated restraint on CRH-BP mRNA in basolateral amygdala (BLA) and dorsal hippocampus (DH), brain regions involved in fear and motivation. Using in situ hybridization, we found that a single acute period of restraint significantly increased CRH-BP mRNA in BLA by 20% but had no effect in DH. Repeated restraint had no effect on basal levels of CRH-BP mRNA in BLA or DH. Importantly, repeated restraint blocked the effects of acute restraint in the BLA. These results demonstrate differential effects of acute and repeated restraint on CRH-BP mRNA.
The contribution of cardiovascular activity in the early central responses to systemic inflammation was assessed in rats following intravenous administration of subseptic doses of lipopolysaccharide (LPS). LPS at 12.5 microg/kg increased heart rate (HR) but did not alter mean arterial pressure (MAP), and induced interleukin-1 beta (IL-1 beta) gene expression at 1 h in circumventricular organs (CVOs), choroid plexus, meninges, blood vessels, and pituitary gland. IL-1 beta mRNA levels were attenuated at 2 h in most regions studied. LPS at 50 microg/kg caused a biphasic change in MAP, increased HR, increased levels of arginine vasopressin heteronuclear RNA in the hypothalamic paraventricular nucleus (PVN), and induced IL-1 beta gene expression in the nucleus of the solitary tract (NTS) at 1 h. LPS (both doses) induced Fos-like immunoreactivity (FLI) in the area postrema, organum vasculosum of the lamina terminalis, NTS, preoptic area, supraoptic nucleus, and PVN at 1 h. In the PVN, neurons with FLI were found primarily in the dorsal and dorsal medial parvocellular divisions after 12.5 microg/kg of LPS whereas neurons with FLI were found throughout the PVN after 50 microg/kg of LPS. After 2 h, FLI was widespread throughout the brain. Plasma ACTH levels were elevated at 1 and 2 h in response to both doses of LPS, and levels of CRF mRNA were increased after 2 h in the parvocellular PVN. Our results reveal that central responses to increasing doses of LPS show different patterns which are related to activation of distinct immune and viscerosensory pathways, and that cardiovascular responses contribute to early neuronal activation as LPS concentrations are increased.