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)

The effects of various neurogenic peptides and neurotransmitter substances on the release of ACTH induced by hypothalamic corticotropin releasing factor (HY-CRF) were investigated using monolayer cultured anterior pituitary cells. Test substances were given in combination with 0.05-0.1 hypothalamic extract (HE)/ml, because HE evoked a significant ACTH release and a linear dose response relationship was demonstrated sequentially between 0.0165 HE/ml and 0.5 HE/ml. Relative high doses of lysine-vasopressin showed a slight additive effect on the release of ACTH induced by 0.1 HE/ml. Leu-enkephalin, dopamine, prostaglandin E1 and E2 slightly reduced the release of ACTH induced by HY-CRF, but the inhibitory effect of these substances were not dose-related. Other tested substances including luteinizing hormone releasing hormone, thyrotropin releasing hormone, somatostatin, melanocyte stimulating hormone release inhibiting factor, beta-endorphin, neurotensin, substance P, vasoactive intestinal polypeptide, angiotensin II, norepinephrine, serotonin, acetylcholine, histamine and gamma-amino butyric acid showed neither agonistic nor antagonistic effect on the release of ACTH induced by HY-CRF. These results indicate that the release of ACTH is controlled specifically by HY-CRF and corticosterone, and modified slightly by some other substances such as vasopressin and prostaglandins, and that the effect of most other neurogenic peptides and neurotransmitter substances is negligible or non-physiological at the pituitary level.
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PMID:ACTH release in pituitary cell cultures. Effect of neurogenic peptides and neurotransmitter substances on ACTH release induced by hypothalamic corticotropin releasing factor (CRF). 3 43

Biologically active peptides and neurotransmitter substances were added to anterior pituitary cell cultures to examine the presence of corticotropin releasing factor (CRF)-like activity. Hypothalamic extract (HE) induced significant dose-related increase of ACTH, and the lowest effective dose was 0.01 HE/ml. Other tested substances including luteinizing hormone-releasing hormone, thyrotropin releasing hormone, melanocyte stimulating hormone release inhibiting factor, somatostatin, substance P, neurotensin, beta-endorphin. leu-enkephalin, met-enkephalin, bradykinin, norepinephrine, dopamine, serotonin, acetylcholine, histamine, gamma-amino butyric acid or gamma-hydroxy butyric acid showed no CRF-like activity. Relatively high doses of lysine vasopressin, arginine vasopressin and angiotensin II increased the release of ACTH in pituitary cell cultures, but the maximal ACTH response was markedly less than with HE. These results indicate that cultured anterior pituitary cells are sensitive and fairly specific in detecting CRF(s) comparing with other detecting procedures.
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PMID:Specificity of cultured anterior pituitary cells in detecting corticotropin releasing factor(s): the effect of biologically active peptides and neurotransmitter substances on ACTH release in pituitary cell cultures. 3 34

Our previous study showed that intracerebroventricular (ICV) administration of corticotropin-releasing hormone (CRH) produced a significant increase in locomotor activity at a dose of 1 microgram and slow stereotypy with prominent grooming at a dose of 10 micrograms. In addition, the ICV administration of CRH caused a significant increase in dopamine (DA) and norepinephrine turnover (NE) in various forebrain regions. The present study was designed to investigate the effects of the ICV administration of CRH on cholecystokinin (CCK), neuropeptide Y (NPY), somatostatin (SOM) and gamma-amino butyric acid (GABA) in the rat forebrain. The ICV administration of 1 and 10 micrograms CRH caused a marked reduction in CCK-like immunoreactivity (CCK-LI), NPY-LI and SOM-LI in the medial frontal cortex (MFC) and anterior cingulate cortex (Ant.CC), whereas it induced an increment of NPY-LI in the nucleus accumbens (NAc) and striatum. Increased SOM-LI and decreased NPY-LI were observed in the hippocampus following the ICV administration of CRH at both doses. The ICV administration of CRH caused a significant decrease in the BAGA content in the MFC, ant.CC, NAc and striatum. Taken together with our previous findings, these results indicate that the ICV administration of CRH induced classical neurotransmitter and neuropeptide abnormalities in the central nervous system which resulted increased emotionality, especially anxiety, in rats.
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PMID:The effects of corticotropin-releasing hormone on peptidergic neurons in the rat forebrain. 168 80

The present study determined whether interleukin-2 (IL-2) and IL-2 receptors are present in the adult rat hypothalamus. In addition, we determined whether IL-2 is involved in the regulation of neurotransmitter release from hypothalamic slices. In the hypothalamus, the highest levels of endogenous IL-2 and IL-2 receptors were localized to the median eminence and arcuate nucleus. Application of exogenous IL-2 to hypothalamic slices produced significant decreases of potassium (25 mM)-evoked [3H]noradrenaline release (24%) without significantly affecting the evoked release of [14C]glutamate, [14C]5-hydroxytryptamine, [3H]dopamine or [3H] gamma-amino butyric acid. In addition, IL-2 increased the potassium-evoked release of methionine-enkephalin (by 78%) and beta-endorphin (by 38%) from hypothalamic slices without affecting the release of leucine-enkephalin. In contrast, the spontaneous release of neurotransmitters and neuropeptides was not affected by exogenous IL-2. Overall, the findings of this study suggest that hypothalamic IL-2 is an endogenous neurokine that may be of consequence to the regulation of hypothalamic function.
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PMID:Interleukin-2 regulates monoamine and opioid peptide release from the hypothalamus. 847 53

Neuropeptide Y (NPY) displays diverse modes of action in the CNS including the modulation of feeding behavior, gonadotropin releasing hormone release, and stress responses. Many of the above physiological actions have been at least partially attributed to actions of NPY on the NPY Y5 receptor subtype. We utilized an antibody directed against the NPY Y5 receptor to characterize the distribution of this receptor in the rat brain. Using Western blot analysis, this antibody recognized a single major band at approximately 57 kD. To further verify the specificity of the antibody, animals were treated for 5 days with antisense oligonucleotides for the Y5 receptor. The antisense treatment significantly reduced food intake and body weight. Furthermore, the Y5 antibody detected a significant decrease in Y5 receptor protein. Y5-like immunoreactivity (-ir) was observed throughout the hypothalamus, thalamus, hippocampus and cortex. Double-label immunofluorescence demonstrated that Y5-ir was colocalized with the following neuronal phenotypes in the hypothalamus, gonadotropin-releasing hormone, neurophysins, corticotropin-releasing hormone, and gamma-amino butyric acid. In addition, functional interactions were demonstrated by the presence of close appositions of NPY fibers with Y5-ir expressing cells. The wide distribution of the Y5 receptor-ir, as well as the colocalization within specific neuronal populations, agrees with the distribution of the Y5 receptor mRNA and the known physiological roles of the NPY/Y5 system. The role of the NPY/Y5 receptor system as a mediator between signals of peripheral energy availability and reproductive neuroendocrine function is discussed.
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PMID:Hypothalamic circuitry of neuropeptide Y regulation of neuroendocrine function and food intake via the Y5 receptor subtype. 1147 18