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

Eight women with prospectively documented premenstrual syndrome (PMS) underwent multiple samplings for estradiol, progesterone, prolactin, cortisol, and plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) during an asymptomatic midcycle (late follicular) and a symptomatic premenstrual (late luteal) phase of the menstrual cycle. Cerebrospinal fluid (CSF) was collected for analysis of MHPG, norepinephrine (NE), 5-hydroxyindoleacetic acid (5-HIAA), dihydroxyphenylacetic acid (DOPAC), gamma-aminobutyric acid (GABA), homovanillic acid (HVA), tyrosine, tryptophan, beta-endorphin, prostaglandins, adrenocorticotropic hormone (ACTH), and arginine vasopressin (AVP). In subsequent months, a dexamethasone suppression test (DST) and a thyrotropin-releasing hormone (TRH) stimulation test were performed during midcycle and premenstrual phases. Significant results included increased CSF concentrations of MHPG in the premenstrual, as compared with the midcycle, phase of the cycle, and increased plasma cortisol concentrations during the midcycle phase. The DST showed a 62% overall rate of nonsuppression, irrespective of menstrual cycle phase. Though there were no abnormalities of thyrotropin-stimulating hormone (TSH) after TRH stimulation, the mean delta maximum prolactin values after TRH stimulation were higher than reported normal values both at midcycle and premenstrually. These pilot data suggest hormonal axes that might be worthy of further systematic investigation in future studies of PMS.
 ...
PMID:CSF and endocrine studies of premenstrual syndrome. 193 Jun 15

To evaluate the neurochemical, neuroendocrine, and behavioral effects of exogenous corticosteroids in humans, we administered prednisone (80 mg/d orally for 5 days) in a double-blind manner to 12 medically healthy volunteers. Behavioral measures were assessed before, during, and after prednisone administration in all 12 subjects, and cerebrospinal fluid biochemistry was assessed before and during prednisone administration in 9 of the subjects. Prednisone administration was associated with decreases in cerebrospinal fluid levels of corticotropin, norepinephrine, beta-endorphin, beta-lipotropin, and somatostatinlike immunoreactivity. No significant changes were noted in cerebrospinal fluid levels of alpha-melanocyte-stimulating hormone, corticotropin-releasing hormone, 3-methoxy-4-hydroxyphenylglycol, homovanillic acid, or 5-hydroxyindoleacetic acid. No consistent or significant group mean changes were observed in structured behavioral ratings, although 9 (75%) of the volunteers studied reported mild behavioral changes while receiving prednisone. Correlations between the neurochemical and behavioral changes are discussed.
 ...
PMID:Prednisone effects on neurochemistry and behavior. Preliminary findings. 197 71

Baseline concentrations of beta-endorphin (beta-EP) and monoamine metabolites (MHPG: 3-methoxy-4-hydroxy-phenylglycol, HVA: homovanillic acid, 5-HIAA: 5-hydroxyindoleacetic acid) in lumbar CSF (LCSF) and ventricular CSF (VCSF) were measured in 18 patients with intractable pain; 10 with deafferented pain and 8 with peripheral pain. Control values were obtained from 37 individuals of various ages. Changes in the concentrations of these substances were determined before and after giving stimulations (2-5 V, 0.2-0.5 msec, 40-50 Hz, 20-sec duration) to 6 patients through electrodes implanted in deep brain structures (DBS; posterior limb of the internal capsule in 5 patients and rostral mesencephalic lemniscus medialis in one patient), and to 2 other patients through electrodes implanted in the spinal dorsal column (DCS). The control value of beta-EP in LCSF was 57.6 +/- 24.7 pg/ml, which was not significantly different from that of VCSF. Great variation in the individual control LCSF beta-EP concentrations was found, but it was not related to differences in age. The mean baseline LCSF beta-EP concentration was significantly higher (p less than 0.05) than the control in the patients with deaffernted pain before stimulation. One of the monoamine-metabolites, MHPG, showed higher level in the patients with peripheral pain (p less than 0.01). The LCSF beta-EP concentration was not affected by deep brain stimulation, but was increased by dorsal column stimulation. In one patient with excellent pain relief by stimulation of the posterior limb of the internal capsule, the LCSF HVA and 5-HIAA concentrations were conspicuously increased.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[beta-Endorphin and monoamine metabolite concentrations in patients with intractable pain--changes before and after deep brain or spinal dorsal column stimulation]. 241 30

Cerebrospinal fluid (CSF) homovanillic acid, 5-hydroxyindoleacetic acid, 3-methoxy-4-hydroxyphenylglycol, and somatostatin and beta-endorphin levels were measured in 12 patients with panic disorder before and after 7 months of treatment with alprazolam or imipramine. The concentrations of CSF monoamine metabolites and neuropeptides were at baseline of the same order of magnitude in panic patients and controls. Neither alprazolam nor imipramine changed metabolite or neuropeptide levels in CSF despite clinical improvement in both treatment groups. According to present CSF data, the antipanic actions of alprazolam and imipramine do not involve the monoaminergic or peptidergic systems studied.
 ...
PMID:Long-term effects of alprazolam and imipramine on cerebrospinal fluid monoamine metabolites and neuropeptides in panic disorder. 248 80

We have examined the presence of 5-hydroxytryptamine (serotonin; 5-HT) in the intermediate lobe of the frog pituitary and investigated the effect of exogenous 5-HT on alpha-melanocyte-stimulating hormone (alpha-MSH) release from the perifused neurointermediate lobe (NIL). Using a specific antiserum against 5-HT, the indirect immunofluorescence technique revealed the presence of 5-HT-like immunoreactivity (5-HT-LI) in discrete cells, generally gathered in small clusters among parenchymal cells, and in numerous neurites surrounding melanotrophic cells. At the electron microscopic level, using a silver-gold intensification procedure, 5-HT-LI was localized in dense-core secretory vesicles within specific pituitary cells which appear to be different from pituitary melanotrophs. Dense accumulation of gold particles was also observed in nerve fibres running between parenchymal cells. A combination of high-performance liquid chromatography analysis and electrochemical detection showed the presence of both 5-HT and its metabolite 5-hydroxyindol acetic acid (5-HIAA) in frog NIL extracts (534 +/- 40 and 1245 +/- 65 (S.E.M.) pg/mg wet tissue respectively). Administration of graded doses of 5-HT (from 1 to 30 mumol/l) to perifused frog NIL induced a dose-dependent inhibition of alpha-MSH release. Repeated pulses of 5-HT (10 mumol/l each) induced a reproducible inhibition of alpha-MSH without any desensitization phenomena. The inhibitory effect of 5-HT was partially blocked by the serotonergic antagonists methysergide and ICS-205-930 (10 mumol/l each). Concomitant administration of methysergide and ICS-205-930 (10 mumol/l each) totally abolished 5-HT-evoked inhibition of alpha-MSH. Fenfluramine, a releaser of 5-HT, induced a slight but significant reduction of alpha-MSH secretion. While 5-HT caused a marked inhibition of alpha-MSH release from intact NIL, 5-HT was devoid of effect on acutely dispersed pars intermedia cells suggesting that 5-HT does not exert a direct action on pituitary melanotrophs. We have examined the effect of specific dopaminergic, GABAergic and alpha-adrenergic antagonists on 5-HT-induced alpha-MSH inhibition. We observed that sulpiride and SR 95531 (10 mumol/l each) did not affect the response of NIL to 5-HT while yohimbine (10 mumol/l) suppressed the inhibitory action of 5-HT. Taken together, our results indicate that discrete cells of the frog pars intermedia contain the neurotransmitter 5-HT which may act locally to inhibit alpha-MSH release.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Effect of serotonin on alpha-melanocyte-stimulating hormone secretion from perifused frog neurointermediate lobe: evidence for the presence of serotonin-containing cells in the frog pars intermedia. 254 46

The therapeutic action of vigabatrin (gamma vinyl GABA, GVG) has been reported to be mediated by GABAergic neurotransmission. In the present study, we evaluated different neurotransmitter systems in the cerebrospinal fluid (CSF) of patients with complex partial epilepsy, before and during GVG treatment. The markers of the GABAergic system (free GABA, total GABA, homocarnosine) showed a two- to threefold elevation. There was also an increase in glycine during the 6 months of GVG treatment. In contrast, we did not find any constant CSF changes in either excitatory amino acids or in markers of the cholinergic (acetylcholinesterase), dopaminergic (homovanillic acid), serotonergic (5-hydroxyindoleacetic acid), or peptidergic (somatostatin, prolactin, beta-endorphin) systems. This finding (except an elevation in glycine) was in agreement with previous studies which suggest a specific action of GVG on the GABAergic system. The role of glycine in antiepileptic efficacy of GVG needs further evaluation.
 ...
PMID:Specificity of vigabatrin for the GABAergic system in human epilepsy. 276 15

The serotonin (5-hydroxytryptamine, 5-HT) precursor 5-hydroxy-L-tryptophan (5-HTP) and 5-HT antagonists, respectively, are able to stimulate and block pituitary adrenocorticotropin (ACTH) release. However, our previous data do not support a role of central serotoninergic systems in the neural control of ACTH release. We thus examined the hypothesis that 5-HTP given either alone or with uptake-blocking drugs such as fluoxetine caused stimulation of ACTH through activation of central noradrenergic neuronal activity (NNA). The hypothesis was tested in normal adult male rats by correlating medial basal hypothalamic NNA and serotoninergic neuronal activity (SNA) with serum ACTH following administration of 5-HTP (20 and 100 mg/kg, i.p.) in the presence or absence of fluoxetine (10 mg/kg, i.p.) or cyproheptadine (10 mg/kg, i.p.). The alpha 2-adrenergic agonist clonidine (150 micrograms/kg, i.p.) was used to inhibit central NNA and to examine the role of alpha 2-adrenoceptors in the actions of serotoninergic drugs. Computerized mass spectrometry was employed to specifically and precisely assay hypothalamic norepinephrine (NE), 3,4-dihydroxyphenylethyleneglycol (DHPG), 5-HT and 5-hydroxyindoleacetic acid (5-HIAA) to obtain indices of hypothalamic NNA (DHPG/NE) and SNA (5-HIAA/5-HT). The administration of fluoxetine/5-HTP stimulated (p less than 0.01) both hypothalamic NNA and ACTH release.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Mechanisms of 5-hydroxy-L-tryptophan-induced adrenocorticotropin release: a major role for central noradrenergic drive. 284 May 94

The neurobehavioral responsiveness of two strains of rats, Fischer-344 (CDF) and Sprague-Dawley (CD), to a repeated foot-shock-induced analgesia (FSIA) stress was compared in this study. Rats were either restrained or freely moving during shock presentation (sham controls were exposed to the shock environment only). The foot-shock (15-s, 1.5-mA scrambled electric shock) was observed to induce analgesia in the CDF, but not the CD strain following acute presentation; analgesia was evaluated using time for tail-withdrawal from hot water (55 degrees C). Both strains exhibited an analgesic response when latency to tail withdrawal was evaluated just prior to daily FSIA presentations over 15 total sessions indicating that these rat strains were behaviorally conditioned to this repeated stressor. However, the levels of conditioned analgesic responses to foot-shock were: greater in the CDF and most evident when rats were restrained on the shock-grid while being administered the foot-shock. All rats were quickly sacrificed following the 15th conditioning session to determine the effects of this stressor on neurotransmitter and neuroendocrine function in both strains of rat. Experimental subjects were exposed to the shock grid but not shocked during this last session. The following was found: plasma corticosterone (CORT) and prolactin levels and adrenal CORT levels were significantly increased by repeated stress in the CDF strain; only plasma CORT levels were elevated in the CD rat; pituitary immunoreactive beta-endorphin levels were significantly higher (+46%) amongst all experimental groups in the CDF strain, but stress was not observed to alter peptide steady-state levels in either strain; dopamine (DA), 5-hydroxytryptamine and metabolites (5-hydroxyindoleacetic acid and dihydroxyphenylacetic acid) levels were generally higher in the hypothalamus and frontal cortex of the CDF rat but turnover rates (implied from metabolite/amine ratios) indicated that these systems were more sluggish in this rat strain; hypothalamic DA turnover was significantly attenuated by repeated FSIA + restraint in both strains, but the dynamics of this effect appeared to be different between rat strains; and frontal cortex 5-HT turnover was significantly elevated by repeated FSIA + restraint in only the CDF rat. This research indicates that the CDF rat is extremely sensitive to an acute FSIA stress and it is less able than the CD rat to adapt to repeated presentation of this stress.
 ...
PMID:Neuroendocrine, biogenic amine and behavioral responsiveness to a repeated foot-shock-induced analgesia (FSIA) stressor in Sprague-Dawley (CD) and Fischer-344 (CDF) rats. 294 19

A local injection of kainic acid (KA) into the dorsal raphe nucleus (NRD) increased the motor activity and produced head shakes, hind limb abduction, forepaw treading and sniffing. This syndrome was antagonized partly by cyproheptadine and completely by naloxone. An injection of KA into the median raphe nucleus (NRM) produced sedation, catalepsy and analgesia, which were accompanied by a decrease in the beta-endorphin immunoreactivity in the mesencephalon. Naloxone completely reversed the behavioral inhibition after KA injections into the NRM, while a pretreatment with cyproheptadine augmented the catalepsy. KA injected into the NRD and NRM depressed the forebrain level of serotonin and slightly elevated that of 5-hydroxyindoleacetic acid. The results demonstrate that besides serotonin the opioid system is also involved in various effects induced by activation of the raphe nuclei.
 ...
PMID:Different behavioral responses of rats to kainate injections into the dorsal and median raphe nuclei. 295 46

The raphe nuclei [which contain serotonin (5-HT) cell bodies] are also known to contain axons that store substance P, met-enkephalin, and gamma-aminobutyric acid (GABA). We have previously shown that GABA has a tonic inhibitory action on 5-HT turnover. To examine other possible interactions of these neuronal systems, we assessed the effect on 5-HT turnover of injecting substance P and 2-D-ala-met-enkephalin into the median raphe nucleus, and the effects of substance P on GABA turnover. Serotonin turnover was increased by 30% in the hippocampus after the injection of substance P (4 micrograms) into the median raphe, indicating an excitatory effect of substance P on the raphe-hippocampal system. Local injection of the metabolically stable metenkephalin analog 2-D-ala-met-enkephalin amide (10 micrograms) increased the hippocampal steady state content of 5-hydroxyindoleacetic acid (5-HIAA) by 60%. The data suggest an excitatory effect of met-enkephalin within the raphe nucleus. We attempted to estimate GABA turnover from the rate of disappearance of GABA after inhibition of glutamic acid decarboxylase by isoniazid and by the rate of accumulation of GABA after inhibition of GABA transaminase by gabaculine. Isoniazid, which is a competitive inhibitor, had too short and incomplete an action to be of use when injected intranuclearly. Gabaculine, which is an irreversible inhibitor, induced a rapid-onset increase in GABA content. This accumulation was linear up to 90 min. The injection fo gabaculine (80 ng) into the raphe increased GABA content by five times the control values, but hippocampal 5-HT and 5-HIAA contents were not significantly changed. Substance P injection increased the GABA turnover by 30%. Gabaculine seems a promising tool for detecting changes in GABA turnover.
 ...
PMID:Serotonin and gamma-aminobutyric acid turnover after injection into the median raphe of substance P and D-ala-met-enkephalin amide. 617 97


<< Previous 1 2 3 4 5 6 Next >>