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 present study was designed to examine the adrenocorticotropic hormone (ACTH) response to N-methyl-D-aspartate (NMDA) in neonatal rats. Subcutaneous injection of NMDA (30 mg/kg) was found to increase plasma ACTH concentrations two-fold after 15 min in 9-10 and 20-21 day-old female and male rats. Pretreatment with the competitive NMDA receptor antagonist CPP (10 mg/kg) failed to attenuate the ACTH response to NMDA in the younger rats, yet reduced the response in older ones. These findings indicate that NMDA can elevate plasma ACTH in both female and male neonatal rats, however this response is not sensitive to CPP antagonism until the end of the neonatal period.
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PMID:Systemic NMDA treatment increases plasma ACTH in the neonatal female and male rat. 132 82

The aim of this study was to elucidate the effects of N-methyl-D-aspartic acid (NMDA) receptor stimulation on the release of several hormones known to be activated during stress. The experiments were performed in conscious freely moving cannulated rats. Systemic administration of N-methyl-D,L-aspartic acid (NMA) and of NMDA in low doses (2.5-10 mg/kg i.p.) was found to induce a dose-related stimulation of adrenocorticotropin (ACTH) release. NMA-induced ACTH release was reduced by administration of an NMDA receptor antagonist (D,L-2-amino-5-phosphonovaleric acid). NMDA was much more potent in activating ACTH release than the racemic form of the amino acid, NMA. In the dose range used, both NMA and NMDA failed to influence prolactin release. With the exception of a small increase in epinephrine concentration in response to the highest dose of NMDA (10 mg/kg), no changes in plasma catecholamines were observed. The data indicate that NMA and NMDA administered in low doses trigger ACTH release without induction of a nonspecific stress response.
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PMID:Stimulation of adrenocorticotropin but not prolactin and catecholamine release by N-methyl-aspartic acid. 166 Sep 64

The present study evaluated the effects of high K+ and four excitatory amino acids (EAAs) on the release of met-enkephalin-like immunoreactivity (ME-i.r.) from slices of the rat striatum and globus pallidus. High K+ (15-50 mM) increased the release of ME-i.r. in a concentration-dependent manner in both regions, the release response in the globus pallidus being consistently greater than in the striatum. This release was highly Ca(++)-dependent and was significantly enhanced in the absence of external Mg++. D-2-Amino-7-phosphonoheptanoic acid (0.5 mM), a competitive N-methyl-D-aspartate (NMDA) receptor antagonist, did not alter this enhanced action of K+, suggesting that the activation of NMDA receptors by an endogenous agonist did not contribute to the enhancement. Exposure of pallidal or striatal slices to four EAA receptor agonists, NMDA, L-glutamate, kainate (KA) and quisqualate, increased the release of ME-i.r. above the base line, an effect that was Ca(++)-dependent. Both L-glutamate and NMDA, at concentrations of 1 and 5 mM, produced a graded increase in the ME-i.r. release, but a higher concentration (10 mM) produced a lower release. In both regions the NMDA (5 mM)-evoked release was effectively inhibited by Mg++ (1.2 mM), 3-(2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid (CPP) (5 microM), a competitive NMDA receptor antagonist and thienylcyclohexylpiperidine (10 microM), a noncompetitive NMDA receptor antagonist. Tetrodotoxin (0.3 microM), a Na+ channel blocker, did not affect the NMDA-evoked release of ME-i.r. in the striatum, but decreased it by 52% in the globus pallidus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Met-enkephalin release from slices of the rat striatum and globus pallidus: stimulation by excitatory amino acids. 167 84

Excitatory amino acids have been known to increase pituitary secretion of LH in vivo and are probably involved in the neuroendocrine regulation of the hypothalamic-pituitary-gonadal axis. We have found that systemic administration of the excitatory amino acid agonist N-methyl-D-aspartate (NMDA) evokes a transient and profound increase in circulating levels of ACTH as well. Treatment of adult male Long-Evans rats with NMDA (30 mg/kg, sc) maximally increased plasma ACTH and immunoreactive beta-endorphin from 7-15 min after injection, and levels of both remained significantly elevated until 60 min into the time course. Corresponding increases in corticosterone were observed 15 and 30 min after treatment, while LH, similar to other pituitary hormones, was increased from 7-30 min after NMDA. Stimulation of the pituitary-adrenal and pituitary-gonadal neuroendocrine axes by NMDA was monitored in subsequent studies by plasma ACTH and LH, respectively; both were increased in a dose-related manner after the administration of 3-60 mg/kg NMDA, although stimulation of ACTH (800%) was more pronounced than that of LH (200%). The increases in ACTH and LH due to NMDA were inhibited by pretreatment with the competitive NMDA antagonist (+/-)3-(2-carboxypiperazin-4- yl)propyl-1-phosphonic acid, CPP (6 and 10 mg/kg, ip, for 21 min); by contrast, dexamethasone pretreatment (50 micrograms/kg, ip, for 4 h) blocked only the NMDA-evoked increase in circulating ACTH. These findings indicate that an NMDA receptor mechanism might be involved in the acute activation of the hypothalamic-pituitary-adrenal axis in the rat.
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PMID:N-methyl-D-aspartate treatment increases circulating adrenocorticotropin and luteinizing hormone in the rat. 184 4

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

The antinociception induced by morphine but not beta-endorphin, D-Pen2-D-Pen5-enkephalin (DPDPE), or U50, 488H (trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl) cyclohexyl] benzeocetamide) administered intracerebroventricularly (i.c.v.) has been previously demonstrated to be mediated by the N-Methyl-D-Aspartic Acid (NMDA) receptor. The present study was designed to determine if non-NMDA receptors are involved in opioid-induced antinociception. Antinociception was assessed by the tail-flick test in male ICR mice. Various doses of CNQX (6-Cyano-7-nitroquinoxaline-2,3-dione), a competitive non-NMDA receptor antagonist, (0.001 to 0.5 microgram) injected intracerebroventricularly (i.c.v.) alone did not show any antinociceptive effect. CNQX (0.01 to 1 micrograms, i.c.v.) dose-dependently attenuated the inhibition of the tail-flick response induced by morphine (1 microgram). However, inhibition of the tail-flick response induced by i.c.v. administered beta-endorphin (1 microgram), DPDPE (10 micrograms), or U50, 488H was not affected by i.c.v. administered CNQX. It is concluded that non-NMDA receptors are involved in i.c.v. morphine-induced antinociception. However, non-NMDA receptors are not involved in i.c.v. administered beta-endorphin-, DPDPE-, and U50, 488H-induced antinociception at the supraspinal level.
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PMID:Non-NMDA receptor antagonist attenuates antinociception induced by morphine but not beta-endorphin, D-Pen2-D-Pen5-enkephalin, and U50, 488H administered intracerebroventricularly in mice. 774 56

The role of the endogenous opioid peptide dynorphin (1-17) in regulating NMDA receptor-mediated synaptic currents was examined in guinea pig hippocampus. Schaffer collateral/commissural fiber-evoked NMDA synaptic currents were recorded using whole-cell patch-clamp techniques in CA3 pyramidal cells. Dynorphin was found to have dual effects on NMDA synaptic currents, increasing currents at low concentrations and decreasing currents at high concentrations. Only the inhibitory action of dynorphin was sensitive to naloxone, indicating that this effect was mediated by an opioid receptor. The inhibitory effect was mimicked by bremazocine, but not by U69,593, U50,488, [D-Ala2, N-Me-Phe4, Gly-ol]-enkephalin, or [D-Pen2,5]-enkephalin. Bremazocine's effect was blocked by naloxone, but not by nor-binaltorphimine, cyprodime, or naltrindole. These findings suggest that bremazocine's effect was mediated by the kappa 2 subtype of opioid receptor. In addition, 1 microM naloxone and antisera to dynorphin (1-17) were found to increase NMDA-mediated synaptic currents. Nor-binaltorphimine, cyprodime, naltrindole, and antisera to met-enkephalin did not increase the NMDA synaptic current. These findings suggest that endogenous dynorphin was acting at kappa 2 receptors to inhibit NMDA receptor-mediated synaptic currents. Overall, these findings indicate that dynorphin is an endogenous agonist for kappa 2 receptors in the CA3 region of the guinea pig hippocampus and that these receptors regulate NMDA receptor function.
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PMID:Kappa 2 opioid receptors inhibit NMDA receptor-mediated synaptic currents in guinea pig CA3 pyramidal cells. 791 46

The non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist dizocilpine maleate (MK-801) stimulates the secretion of adrenocorticotropin hormone (ACTH). As corticotropin-releasing factor (CRF) represents the primary modulator of this secretion, we tested the hypothesis that the ability of MK-801 to activate the hypothalamic-pituitary-adrenal (HPA) axis was modulated through actions at the hypothalamic level that modulate the secretion of CRF. Induction of the immediate-early gene c-fos, as well as of CRF mRNA within the paraventricular nucleus (PVN) of the rat hypothalamus, was examined following the intraperitoneally administration of MK-801 (1 mg/kg). MK-801 markedly increased the expression of Fos-like protein in parvocellular nerve cells of the PVN within 60 min of systemic treatment, and double labeling immunocytochemistry indicated that Fos was primarily localized in CRF-containing neurons of the PVN. MK-801 also significantly increased CRF biosynthesis as detected by in situ hybridization, thus suggesting that c-fos could be involved in the regulation of CRF genes. Taken together, these results suggest that MK-801 stimulates the rat HPA axis probably through the neuronal gene expression of PVN CRF. The significance of these data is discussed in terms of hypothalamic NMDA receptor blockade and subsequent transcriptional regulation of CRF by immediate-early genes.
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PMID:Induction of c-fos and CRF mRNA by MK-801 in the parvocellular paraventricular nucleus of the rat hypothalamus. 796 57

Ifenprodil--an antagonist at the modulatory site of the NMDA receptor complex sensitive to polyamines--intraperitoneally injected at doses of 3 or 10 mg/kg, dose dependently prevented the behavioral syndrome induced by intracerebroventricular administration of adrenocorticotropin (ACTH)-(1-24) in adult male rats (excessive grooming, stretching, yawning, penile erections). These data further support a role of the brain ornithine decarboxylase (ODC)-polyamine system in the ACTH-induced behavioral syndrome, and may suggest an involvement of excitatory amino acids.
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PMID:Influence of ifenprodil on the ACTH-induced behavioral syndrome in rats. 814 97

The binding characteristics of histogranin (HN), an endogenous peptide first recognized for its antagonism of N-methyl-D-aspartate (NMDA) responses, were determined in membrane preparations of rat brain. [125I][Ser1]HN, a stable bioactive analog of HN, bound specifically and reversibly to a homogenous population of high-affinity sites with a Kd of 25 nM and a Bmax of 410 fmol/mg protein. The binding of [125I][Ser1]HN increased linearly with membrane protein concentration and was destroyed upon membrane pretreatment with trypsin. The binding displayed rapid association and dissociation kinetics and was blocked by peptides possessing close homology with HN in the following order: [Ser1]HN-(1-15) > HN > [Ser1]HN-(1-14) > HN-(2-15) > [Ser1]-HN-(1-10) > HN-(6-10). Unrelated peptides such as substance P, beta-endorphin, neuropeptide Y, [Met5]enkephalin, [Leu5]enkephalin, dynorphin A(1-13) and neuromedin C were inactive in competition binding assays against [125I]Ser1]HN. Ligands of the binding domains of the NMDA receptor, such as (+)3-(2-carboxypiperazin-4-yl)propyl-1-phosphonic acid, (+) 5-methyl-10,11-dihydro 5H-dibenzo[a, d]cyclohepten-5,10-imine hydrogen maleate, 1-N-(2-thienyl)cyclohexylpiperidine, glycine and glutamate were also ineffective in competing for [125I][Ser1]HN binding sites. Interestingly, specific ligands for the polyamine site on the NMDA receptor, as well as the cations Mg++ and Zn++ inhibited [125I][Ser1]HN binding. The polyamine antagonist diethylenetriamine produced a noncompetitive inhibition with an IC50 (175 nM) comparable to that of HN (75 nM). The cations Zn++ and Mg++ displaced [125I][Ser1]HN binding with IC50 values of 18 and 240 microM, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characterization of [125I][Ser1]histogranin binding sites in rat brain. 822 61


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