Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gonadal steroids exert a powerful regulatory influence upon the functioning of gonadotropin-releasing hormone (GnRH) neurons despite the apparent absence of gonadal steroid receptors in these cells. By using retrograde-tracing techniques combined with dual-labeling immunocytochemistry, we show here that distinct populations of estrogen receptor alpha (ERalpha)-containing neurons located in the hypothalamus and caudal brainstem project to the vicinity of the GnRH perikarya located in the rostral preoptic area (rPOA). The strongest estrogen-receptive afferent projection to this area originated from neurons located in the anteroventral periventricular and medial preoptic nuclei of the preoptic area. Approximately 50% of arcuate nucleus neurons projecting to the rPOA were demonstrated to synthesize either neuropeptide Y or beta-endorphin, but little evidence was found for ERalpha immunoreactivity in either of these specific subpopulations. Over 80% of all tyrosine hydroxylase-expressing neurons in the arcuate nucleus expressed ERalpha, but none projected to the rPOA. In the caudal brainstem, the A1 and A2 norepinephrine neurons comprised nearly all of the retrogradely labeled neurons. However, only the A2 afferents expressed ERalpha immunoreactivity, whereas the A1 afferents coexpressed neuropeptide Y. These observations, combined with the anterograde labeling data of others, provide neuroanatomical evidence for the existence of specific estrogen-receptive neuronal cell populations that project to the rPOA and may be involved in the estrogen-dependent transsynaptic regulation of GnRH neurons in the rat.
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PMID:Identification and characterization of estrogen receptor alpha-containing neurons projecting to the vicinity of the gonadotropin-releasing hormone perikarya in the rostral preoptic area of the rat. 1040 58

Food restriction is associated with a number of endocrine disturbances. We validated the experimental conditions for several house-keeping genes and determined the effects of 12 day 50% food restriction on hypothalamic and pituitary transcription of genes involved in different neuroendocrine systems, using real-time quantitative polymerase chain reaction (PCR). A total of 7 nuclear receptors and 12 neuropeptides and peptide hormones were investigated in the dorsal and ventral hypothalamus and the pituitary gland in rats. In the hypothalamus, food restriction reduced mRNA levels of estrogen receptor alpha (ERalpha), progesterone receptor, glucocorticoid receptor, thyroid hormone receptor alpha and beta, pro-opiomelanocortin (POMC), growth hormone-releasing factor (GHRF), corticotropin-releasing factor (CRF), thyrotropin-releasing factor (TRF), somatostatin, and increased that of neuropeptide Y (NPY). In the pituitary, the treatment reduced growth hormone (GH), luteinizing hormone beta (LHbeta) and thyrotropin beta, but increased ERalpha mRNA levels. The study provides a map of how food restriction affects the regulation of a number of transcripts involved in neuroendocrine control.
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PMID:Differential regulation of nuclear receptors, neuropeptides and peptide hormones in the hypothalamus and pituitary of food restricted rats. 1566 63

Numerous studies have established a link between individuals with affective disorders and a dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis, most notably characterized by a reduced sensitivity to glucocorticoid negative (-) feedback. Furthermore there is a sex difference in the etiology of mood disorders with incidence in females being two to three times that of males, an association that may be a result of the influence of estradiol (E2) on HPA axis function. In these studies, we have examined the effect of E2 on glucocorticoid-mediated HPA axis (-) feedback during both the diurnal peak and the stress-induced rise in corticosterone (CORT). Young adult female Sprague-Dawley (SD) rats were ovariectomized (OVX) and 1 week later treated subcutaneous (s.c.) with oil or estradiol benzoate (EB) for 4 days. On the 4th day of treatment, animals were injected with a single dose of dexamethasone (DEX), or vehicle. EB treatment significantly increased the evening elevation in CORT and the stress-induced rise in CORT. In contrast, DEX treatment reduced the diurnal and stress induced rise in CORT and adrenocorticotropic hormone (ACTH), and this reduction was not apparent following co-treatment with EB. To determine a potential site of E2's action, female SD rats were OVX and 1 week later, wax pellets containing E2, the estrogen receptor beta (ERbeta) agonist diarylpropionitrile (DPN), or the estrogen receptor alpha (ERalpha) agonist propylpyrazoletriol (PPT), was implanted bilaterally and dorsal to the paraventricular nucleus of the hypothalamus (PVN). Seven days later, animals were injected s.c. with a single dose of DEX, or vehicle to test for glucocorticoid-dependent (-) feedback. Results show that E2 and PPT increased, while DPN decreased the diurnal peak and stress-induced CORT and ACTH levels as compared to controls. Furthermore, E2 and PPT impaired the ability of DEX to inhibit both the diurnal and the stress-induced rise in CORT and ACTH, whereas DPN had no effect. Neuronal activation was measured by c-fos mRNA expression within the PVN following restraint. E2 and PPT increased c-fos mRNA, and impaired the normal DEX suppression of neuronal activation in the PVN. Taken together, these data indicate that estradiol causes a dysregulation of HPA axis (-) feedback as evidenced by the inability of DEX to suppress diurnal and stress-induced CORT and ACTH secretion. Additionally, the ability of E2 to inhibit glucocorticoid (-) feedback occurs specifically via ERalpha acting at the level of the PVN.
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PMID:Estrogen impairs glucocorticoid dependent negative feedback on the hypothalamic-pituitary-adrenal axis via estrogen receptor alpha within the hypothalamus. 1916 15

The purpose of this study was to evaluate the effects of stress and estradiol (E2) on pain tolerance. Ovariectomized rats were assigned to treatment groups based on a 2 x 4 factorial design comprising stress (nonstress x stress) and hormone treatment vehicle x E2 [0.25 mg/kg/d]) x estrogen receptor alpha (ERalpha)-selective agonist propyl pyrazole triol (1 mg/kg/d) x estrogen receptor beta (ERbeta)-selective agonist diarylpropionitrile (1 mg/kg/d). Stressed animals underwent daily 60-minute immobilization for 22 days. Pain tolerance was assessed with the hot plate test, an acute thermal pain test. In this study, stressed rats showed increased (P < .05) pain tolerance compared with nonstressed rats (25.0 +/- 1.92 s vs 20.4 +/- 1.02 s, respectively). Increased (P < .05) pain threshold was observed in nonstressed and stressed rats treated with E2 and the ERalpha agonist compared with vehicle-treated rats. Interestingly, the ERbeta agonist only increased (P < .10) pain thresholds in stressed rats. Stressed rats exhibited higher (P < .05) beta-endorphin levels compared with nonstressed rats in all hormone-treatment groups. With the exception of stressed rats treated with the ERbeta agonist, there was no hormone effect on beta-endorphin levels. These studies suggest that E2's effect on pain thresholds may be mediated via the ERalpha, while the interaction between chronic stress and ERbeta may also enhance pain threshold.
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PMID:Effects of immobilization stress and hormonal treatment on nociception. 2325 66