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)

In summary, 5HT, ACh, NE, E and DA appear to stimulate hypothalamic CRH secretion whereas activation of the GABA/BZD system seems to decrease the responsivity of the CRH neuron to stimulatory neurotransmitters (Fig. 6). Hypothalamic CRH released from the hypothalamic neuron not only activates the HPA axis, but also stimulates the locus coeruleus-norepinephrine system (LC) and the central sympathetic system (CSS). CRH also induces secretion of hypothalamic POMC gene-derived peptides, such as ACTH, beta-EP, alpha-MSH and CLIP. These peptides as well as CRH itself, decrease the responsivity of the CRH neuron to stimulatory inputs. In addition, glucocorticoids restrain the activity of both the CRH neuron and the locus coeruleus and may also inhibit the secretion of POMC gene-derived peptides by the POMC neurons of the arcuate nucleus. Hypothalamic CRH secretion is regulated also by a number of mediators of the immune response, such as IL-1, IL-2, TNF-alpha and PGF2 alpha, PAF and EGF. Although the physiologic significance of this regulation is largely unknown, it is tempting to speculate that cytokines and mediators of inflammation released in vivo may activate the HPA axis to trigger a glucocorticoid-mediated counter-regulatory mechanism to restrain the immune system (Fig. 7). (Formula: see text). Fig. 7. Schematic representation of the interactions between the HPA axis and the immune system. Continuous lines represent stimulatory inputs and interrupted lines represent inhibitory inputs. In conclusion, our in vitro hypothalamic organ culture system allowed us to examine the regulation of CRH secretion in a direct and specific manner. Some of our observations may help with better understanding of the role played by CRH in the complex symptomatology of stress. In making extrapolations and interpretations from the in vitro data, however, we should try to keep in mind the words of Claude Bernard, "... If we break up a living organism by isolating its different parts it is only for the sake of ease in analysis and by no means in order to consider them separately. Indeed when we wish to ascribe to a physiological quality its value and true significance we must always refer it to this whole and draw our final conclusions only in relation to the effects in the whole".
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PMID:Regulation of rat hypothalamic corticotropin-releasing hormone secretion in vitro: potential clinical implications. 290 18

Push-pull cannulae were implanted into the preoptic area and into the mediobasal hypothalamic median eminence complex of ovariectomized rhesus monkeys. After recovery, perfusion of the implanted areas was performed over a period of 56 h before and following estradiol benzoate treatment. This treatment results in a drop of LH levels followed by an increase. Catecholamine (norepinephrine, epinephrine and dopamine) concentrations in perfusates collected at 15 min intervals fluctuated tremendously prior to treatment with the estrogen. These fluctuations were largely reduced in perfusates of both structures following the estrogen treatment. They reoccurred at the time of increasing LH levels. beta-endorphin and GABA concentrations were also measured in the perfusates of both structures. Occasional secretory bursts were observed without any obvious relation to the estrogen treatment. It is concluded that catecholamine release in the preoptic area and in the mediobasal hypothalamic median eminence complex is of a pulsatile nature in ovariectomized rhesus monkeys. This pulsatility is largely reduced or abolished following estrogen treatment. The reduced pulsatility may bear a signal character for the release of LH.
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PMID:Release rates of catecholamines, GABA and beta-endorphin in the preoptic area and the mediobasal hypothalamus of the rhesus monkey in push-pull perfusates: correlation with blood hormone levels. 294 31

The action of atrial natriuretic factor (ANF) on alpha-MSH release from frog neurointermediate lobe was studied in vitro using a perifusion technique. Synthetic ANF Arg101-Tyr 126, at concentrations ranging from 10(-7) to 10(-5)M, caused a dose-related stimulation of alpha-MSH release. In addition, dopamine, GABA and NPY, three neuroendocrine factors which inhibit alpha-MSH secretion totally suppressed the action of ANF on alpha-MSH production. The neural lobe of the amphibian pituitary contains numerous ANF immunoreactive fibers, and this regulatory peptide may diffuse from nerves terminating in the pars nervosa to the pars intermedia. Thus, our results suggest that ANF of hypothalamo-neurohypophysial origin may be involved in the multineuronal regulation of amphibian melanotrophs.
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PMID:Atrial natriuretic factor (ANF) stimulates the release of alpha-MSH from frog neurointermediate lobes in vitro. Interaction with dopamine, GABA and neuropeptide Y. 295 56

Resting tremor and hypokinesia of unilateral limbs were produced in monkeys after making a lesion in the mesencephalic tegmentum. The administration of L-dopa or dopamine agonists relieved them and followingly induced dyskinesias. The same effects were produced by the direct injection of dopamine or its agonists into the dorsomedial part of caudate nucleus ipsilateral to the lesion, where spiroperidol binding to the D2 receptor was increased in the affinity. These results suggest that denervation supersensitivity at the postsynaptic D2 receptor is a basic condition for the development of dyskinesias, though they were slightly suppressed by the intracaudate injection of GABA, serotonin and met-enkephalin.
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PMID:Experimental study on resting tremor and L-dopa-induced dyskinesia. 295 3

The effects of calcium hopantenate (HOPA) on plasma beta-endorphin-like immunoreactivity (beta-En-LI) levels in rats have been studied. HOPA (1.5 g/kg) was injected ip, and the animals were serially decapitated. The plasma beta-En-LI levels were measured by radioimmunoassay. Effects of HOPA on beta-En-LI release from the anterior pituitary were also investigated by means of an in vitro experiment. The beta-En-LI content in the hypothalamus and pituitary gland did not change significantly after HOPA injection. The plasma beta-En-LI levels increased significantly in a dose-related manner with a zenith at 30 min after HOPA injection. Effects of HOPA on plasma beta-En-LI levels were prevented with the pretreatment of bicuculline. The beta-En-LI release from the anterior pituitary was enhanced with the addition of HOPA to the medium, and HOPA's effects were blocked with an addition of bicuculline to the medium. These findings suggest that HOPA acts on the anterior pituitary to stimulate beta-En-LI release, and its effects are mediated via GABA receptor.
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PMID:Calcium hopantenate, a GABA agonist, induces elevation of plasma beta-endorphin-like immunoreactivity levels in rats. 295 19

A primary culture of porcine pars intermedia cells with particularly high yields has been developed. The cells, grown in monolayers, secrete the pro-opiomelanocortin-derived peptide alpha-melanocyte-stimulating hormone over several weeks. The patch-clamp technique has been used to demonstrate the presence of gamma-aminobutyrateA (GABAA) receptors on the cells. GABA or the selective GABAA receptor agonist isoguvacine produced a depolarizing increase in chloride conductance that desensitized rapidly. The response was antagonized by bicuculline and by the aminopyridazine derivative of GABA (SR 95103), a novel GABAA receptor antagonist. The effects of specific agonists for each receptor were tested on peptide release from cells maintained in a perfusion system. Isoguvacine (10 microM) potentiated Ba2+-evoked release of alpha-melanocyte-stimulating hormone, whereas (-)-baclofen (50 microM) decreased both basal and stimulated hormone release. This negative effect on peptide secretion was reproduced when GABA (50 microM) was perfused in the presence of bicuculline (10 microM) to block GABAA receptor activation. The possible mechanisms underlying these GABAA and GABAB effects on stimulus-secretion coupling in this neuroendocrine model are discussed.
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PMID:GABAA and GABAB receptors on porcine pars intermedia cells in primary culture: functional role in modulating peptide release. 301 9

The benzodiazepine/GABA receptor coupled chloride ionophore was examined in brain membranes of rats maintained in either a conventional animal facility or a "protected" (low-stress) environment. Following a 10 min ambient temperature swim, animals maintained in both environments had qualitatively similar increases in the number (Bmax) of [35S]t-butylbicyclophosphorothionate (TBPS) binding sites, the apparent affinity of this radioligand, and the efficacy and potency of Cl- to enhance [3H]flunitrazepam binding. Nonetheless, the Bmax of [35S]TBPS and efficacy of Cl- to enhance [3H]flunitrazepam binding were significantly lower in animals housed in the protected environment compared to those maintained in a conventional facility both before and after swim stress. Furthermore, in rats housed in a protected environment, sequential removal of animals from a common cage (cohort removal), produced a very rapid increase (less than or equal to 15 s) in Cl(-)-enhanced [3H]flunitrazepam binding in cortical and hippocampal but not cerebellar membranes. Cohort removal also produced a sequential increase in the number of [35S]TBPS binding sites and apparent affinity of this radioligand in cerebral cortical membranes. The effects of cohort removal were not observed in animals subjected to ambient temperature swim or if animals were removed from different cages. Changes in the benzodiazepine/GABA receptor coupled chloride ionophore produced by cohort removal from a common cage preceded any statistically significant changes in circulating levels of alpha-MSH, beta-endorphin, ACTH or corticosterone. These findings suggest that the benzodiazepine/GABA receptor chloride ionophore complex (supramolecular complex) is under both tonic and acute regulation by the environment, and may subserve a physiologically relevant function in the response to stressful or anxiety producing stimuli.
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PMID:Environmentally-induced modification of the benzodiazepine/GABA receptor coupled chloride ionophore. 303 19

Catecholamines and GABA are neurotransmitters involved in the regulation of release of pro-opiomelanocortin (POMC) derived peptides from the neurointermediate lobe of Xenopus laevis. The present study concerns the relation of these neurotransmitters to the adenylate cyclase system of the melanotrope cell. During in vitro incubation of isolated melanotrope cells it was found that dopamine, adrenaline and LY 171555 induced inhibition of forskolin-stimulated cAMP production and concomitantly inhibited MSH release. Activation of the GABAb receptors by baclofen also induced inhibition of cAMP production and alpha MSH secretion. Activation of the GABAa receptors evoked stimulation of cAMP production, while alpha MSH release was slightly inhibited, indicating that the GABAa mechanism may prove to be complex. A dual regulation through two subtypes of this receptor might be involved, one stimulating release through the adenylate cyclase system, while the other would inhibit secretion.
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PMID:Regulation of cyclic-AMP synthesis in amphibian melanotrope cells through catecholamine and GABA receptors. 303 16

The action of the central-type benzodiazepine-receptor agonist clonazepam on alpha-MSH release has been studied in vitro using perifused frog neurointermediate lobes. High concentrations of clonazepam (3.16 X 10(-5) and 10(-4) M) caused an inhibition of alpha-MSH release and this effect was reversed by the central-type benzodiazepine-receptor antagonist Ro 15-1788. High doses of GABA (10(-5) and 10(-4) M) induced a biphasic effect on pars intermedia cells: a brief stimulation followed by a sustained inhibition of alpha-MSH secretion. Administration of clonazepam (10(-5) M) in the presence of various concentrations of GABA (10(-6) to 10(-4) M) led to a potentiation of both stimulatory and inhibitory phases of alpha-MSH secretion induced by GABA. Ro 15-1788 completely abolished the potentiating effect of clonazepam. Thus our results indicate that endogenous benzodiazepine receptors may modulate the effects of GABA on alpha-MSH secretion.
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PMID:The benzodiazepine agonist clonazepam potentiates the effects of gamma-aminobutyric acid on alpha-MSH release from neurointermediate lobes in vitro. 303 17

OFF-center amacrine cells were intracellularly recorded and stained with Lucifer yellow to investigate the cell correlations between photoresponses and morphological features. All OFF-amacrine cells were monostratified and branched within the outer half of the inner plexiform layer. In the flat-mounted retina, however, three distinct morphological classes were distinguishable, which correlated with observed physiological differences. Class 1 consisted of wide-field, stellate amacrine cells with long, thin processes, which branched only close to the soma. The diameter of the circular dendritic field ranged from 0.8 mm to 2.0 mm. Their photoresponse to spot stimulation was a hyperpolarization during light-ON and a small depolarization after light-OFF. They showed strong antagonistic center-surround organization of the receptive field. Its size was approximately equal to the dendritic field size. Class 2 consisted of wide-field, giant amacrine cells with a "central" dendritic field formed by thick dendrites, and a "peripheral" dendritic field formed by a few long and thin, "axonlike" processes. The shape of the dendritic field was elongated, with the long axis parallel to the visual streak. Their receptive field size was considerably smaller than their dendritic field size, which was several millimeters of diameter along the long axis. Their photoresponse to spot stimulation was a fast depolarization after light-OFF, and about 50% of these cells showed strong antagonistic center-surround receptive field organization. Class 3 consisted of small- or medium-field, "starburstlike" amacrine cells with circular dendritic fields of 0.1 mm to 0.6 mm diameter. Their fine, beaded dendrites branched predominantly in the distal parts of the dendritic field. their photoresponses to light were similar to those of the giant amacrine cells; however, their receptive field size exceeded the dendritic field size. Radial sections of the retinas with labeled cells were incubated in antisera to reveal the putative transmitters GABA, serotonin, neurotensin, met-enkephalin and glucagon. No immunoreactivity with these antisera was detected within the stained OFF-center amacrine cells.
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PMID:Physiological and morphological characterization of OFF-center amacrine cells in the turtle retina. 341


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