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 purpose of the present study was to examine the effects of non-NMDA receptor blockade and activation on the activity of tuberoinfundibular dopaminergic (TIDA), periventricular-hypophysial dopaminergic (PHDA) and, for comparison, nigrostriatal dopaminergic (NSDA) neurons in male and female rats. The activity of TIDA, PHDA and NSDA neurons was estimated by measuring the concentration of the primary dopamine metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the median eminence, intermediate lobe of the posterior pituitary and striatum, respectively. Systemic administration of the alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-selective antagonist 6-nitro-7-sulfamoyl-benzo[f]quinoxaline-2,3(1H,4H)-dione (NBQX) increased DOPAC concentrations in the median eminence and intermediate lobe, and decreased plasma concentrations of prolactin and alpha-MSH, in a dose- and time-related manner. In contrast, NBQX had no effect on DOPAC concentrations in the striatum, suggesting that non-NMDA receptors are not involved in the tonic regulation of NSDA neurons. The increase in DOPAC concentrations in the median eminence and intermediate lobe, and the decrease in plasma concentrations of prolactin and alpha-MSH, produced by NBQX were prevented by AMPA but not by kainic acid. Taken together, the results demonstrate that endogenous excitatory amino acid neurotransmitters, acting at AMPA receptors, tonically inhibit both TIDA and PHDA neurons, and thereby increase the secretion of prolactin and alpha-MSH in male and female rats.
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PMID:Non-NMDA receptor-mediated regulation of hypothalamic dopaminergic neurons in the rat. 751 17

A model employing perfusion of artificial cerebrospinal fluid from the lateral ventricle to the cisterna magna in the halothane anesthetized rat was used to study beta-endorphin release in the brain. Injection of 75 micrograms capsaicin into the lumbar intrathecal space released beta-endorphin immunoreactivity into perfusate. The release was blocked by intrathecal pretreatment with 1.25 mg lidocaine and the capsaicin receptor antagonist capsazepine (92 micrograms), showing that the release is caused by binding of capsaicin to a spinal receptor. The release was also blocked by intrathecal pretreatment with the NMDA antagonist MK-801 (3 micrograms) and the NK-1 receptor antagonist CP96,345 (200 micrograms), whereas the AMPA receptor antagonist NBQX (6 micrograms) yielded no significant inhibition. Surprisingly, morphine (30 micrograms) and sufentanil (1.5 micrograms) did not prevent release of beta-endorphin immunoreactivity, although blocking the cardiovascular responses to a noxious heat stimulus. High performance liquid chromatography characterization of perfusates collected after capsaicin injection showed that all beta-endorphin immunoreactivity coeluted with authentic beta-endorphin1-31. beta-Endorphin immunoreactivity in plasma was increased 10 min, but not 25 min, after capsaicin injection. Capsaicin injection abolished the motor and cardiovascular responses to tail immersion in 52.5 degrees C water. Addition of MK-801 (10(-4) mol/l) to the lateral ventricle-cisterna magna perfusate blocked the capsaicin-induced beta-endorphin release, showing that our previous demonstration of an NMDA receptor regulating arcuate nucleus beta-endorphin neuron activity has functional significance. We conclude that in this in vivo, anesthetized preparation including three hot water tail immersions, beta-endorphin can be released into a ventriculo-cisternal perfusate, by activation of the central axons of small primary afferent neurons by capsaicin. These data support the idea that central beta-endorphin may be released in response to prolonged, intense noxious stimulation.
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PMID:Release of beta-endorphin immunoreactivity into ventriculo-cisternal perfusate by lumbar intrathecal capsaicin in the rat. 892 84

A single dose of nicotine given to mice induces first a rapid decrease (presumed release/enhanced degradation) and then a rise (presumed synthesis/enhanced accumulation) of met-enkephalin (Met-Enk) in dorsal and ventral striatum observed at 30 and 60 min post-treatment, respectively. These studies investigated whether the nicotine effect on Met-Enk was mediated indirectly, in part, via other neurotransmitters known to be released by nicotine. Based on the ability of selective antagonists of dopamine (Sch 23390, D1; Sulpiride, D2), glutamate (CPP, competitive NMDA; dizocilpine, non-competitive NMDA; NBQX, AMPA) and GABA (bicuculline, GABA(A); Sch 50911, GABA(B)) receptors, to inhibit or enhance the response to nicotine, we conclude that nicotine alters striatal Met-Enk, in part, via glutamate NMDA and AMPA receptors. These findings further support the notion that glutamate might play a role in the pharmacology of nicotine.
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PMID:Glutamate receptors participate in the nicotine-induced changes of met-enkephalin in striatum. 1099 37

Glutamate is the dominant excitatory neurotransmitter in a large number of physiological processes including neuroendocrine regulation. Some pharmacological studies have shown that different subtypes of glutamate receptor, such as the N-methyl-D-aspartic acid (NMDA) and alpha-amino-3-hydroxy-5-methy-4-isoxazolepropionic acid (AMPA) receptors, are involved in stress-induced adrenocorticotropin (ACTH) and prolactin secretion. However, the roles of the respective glutamate receptors and the mechanism of ACTH and prolactin secretion during stress via these receptors have not been investigated in detail. In the present study, we evaluated the role of AMPA-type glutamate receptor in ACTH and prolactin regulation under restraint stress in adult male rats. Male rats pretreated with a selective AMPA receptor antagonist, 2, 3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX; 50 microg), through a lateral ventricle cannula were stressed by immobilization. Administration of NBQX inhibited ACTH and prolactin secretion in response to restraint stress. However, NBQX had no significant effects on the activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in dopamine biosynthesis, as measured by the accumulation of 3, 4-dihydroxyphenylalanine (DOPA). In addition, administration of NBQX suppressed stress-induced prolactin secretion in the male rats pretreated with alpha-MT, an inhibitor of dopamine synthesis, and infused with dopamine solution (2.5 microg/200 microl/10 min). These results indicated that the effects of NBQX on prolactin secretion might be mediated by non-dopamine mechanisms. The contents of corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP) in the median eminence (ME) of the male rats decreased during restraint stress; however, the fluctuations in CRH and AVP were eliminated by NBQX administration. These results suggest that stress-induced ACTH and prolactin release mediated by neurotransmission via AMPA receptors might be partly attributable to hypophysiotropic regulatory factors in the hypothalamus.
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PMID:Inhibition of stress-induced adrenocorticotropin and prolactin secretion mediating hypophysiotropic factors by antagonist of AMPA type glutamate receptor. 1727 25

We have previously reported that chemical stimulation of the hypothalamic arcuate nucleus (ARCN) in the rat elicited increases as well as decreases in blood pressure (BP) and sympathetic nerve activity (SNA). The type of response elicited from the ARCN (i.e., increase or decrease in BP and SNA) depended on the level of baroreceptor activity which, in turn, was determined by baseline BP in rats with intact baroreceptors. Based on this information, it was hypothesized that baroreceptor unloading may play a role in the type of response elicited from the ARCN. Therefore, the effect of barodenervation on the ARCN-induced cardiovascular and sympathetic responses and the neurotransmitters in the hypothalamic paraventricular nucleus (PVN) mediating the excitatory responses elicited from the ARCN were investigated in urethane-anesthetized adult male Wistar rats. Bilateral barodenervation converted decreases in mean arterial pressure (MAP) and greater splanchnic nerve activity (GSNA) elicited by chemical stimulation of the ARCN with microinjections of N-methyl-D-aspartic acid to increases in MAP and GSNA and exaggerated the increases in heart rate (HR). Combined microinjections of NBQX and D-AP7 (ionotropic glutamate receptor antagonists) into the PVN in barodenervated rats converted increases in MAP and GSNA elicited by the ARCN stimulation to decreases in MAP and GSNA and attenuated increases in HR. Microinjections of SHU9119 (a melanocortin 3/4 receptor antagonist) into the PVN in barodenervated rats attenuated increases in MAP, GSNA and HR elicited by the ARCN stimulation. ARCN neurons projecting to the PVN were immunoreactive for proopiomelanocortin, alpha-melanocyte stimulating hormone (alpha-MSH) and adrenocorticotropic hormone (ACTH). It was concluded that increases in MAP and GSNA and exaggeration of tachycardia elicited by the ARCN stimulation in barodenervated rats may be mediated via release of alpha-MSH and/or ACTH and glutamate from the ARCN neurons projecting to the PVN.
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PMID:Effect of barodenervation on cardiovascular responses elicited from the hypothalamic arcuate nucleus of the rat. 2330 Aug 73