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)

A few examples of hypothalamic, peptidergic disorders leading to clinical signs and symptoms are presented in this review. Increased activity of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus (PVN) and decreased activity of the vasopressin neurons in the biological clock and of the thyroxine-releasing hormone (TRH) neurons in the PVN contribute to the signs and symptoms of depression. In men, the central nucleus of the bed nucleus of the stria terminalis (BSTc) is about twice as large and contains twice as many somatostatin neurons as in women. In transsexuals this sex difference is reversed, pointing to a role of this structure in gender. Luteinizing hormone-releasing hormone (LHRH) neurons are formed in the fetal olfactory placade and migrate along the terminal nerve fibers into the hypothalamus. In Kallmann's syndrome the migration process of the LHRH (gonadotropin-releasing hormone) neurons is aborted, which explains the joint occurrence of hypogonadotropic hypogonadism and anosmia in this syndrome. In postmenopausal women, the neurons of the infundibular nucleus hypertrophy and become hyperactive because of the disappearance of the estrogen feedback and contain hyperactive peptidergic neurons. Climacteric flushes may be caused by hyperactivity of the neurokinin-B or LHRH neurons in this nucleus. The hypocretin (orexin) neurons in the perifornical area are involved in sleep. In narcolepsy with cataplexy, a loss of these neurons, probably due to an autoimmune process, is found. Obese subjects with a mutation in the gene that encodes for leptin, the preproghrelin gene, or the alpha-melanocyte-stimulating hormone (alpha-MSH) gene have been described. Decreased numbers and activity of the oxytocin neurons in the PVN may be responsible for the absence of satiety in Prader-Willi syndrome. Moreover, a glucocorticoid receptor polymorphism is associated with obesitas and dysregulation of the hypothalamus-pituitary-adrenal axis. In contrast, two single nucleotide polymorphisms (SNPs) of the AGRP gene have been associated with anorexia nervosa.
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PMID:Neuropeptides in hypothalamic neuronal disorders. 1554 16

Enkephalin plays a role in the social behaviors of many species, but no corresponding role for this peptide has been investigated in the male Syrian hamster, a species in which brain nuclei controlling social behaviors have been identified. Previous studies have shown the distribution of dynorphin and beta-endorphin throughout social behavior circuits within the male hamster brain. To date, the only studies of enkephalin in the hamster brain address the distribution of this peptide in the olfactory bulb and hippocampus. The present study provides a complete map of enkephalinergic neurons within the forebrain and midbrain of the male Syrian hamster and addresses the question of whether enkephalin immunoreactive (Enk-ir) cells are found within brain regions relevant to male hamster social behaviors. Following immunocytochemistry for either methionine enkephalin (met-enkephalin) or leucine enkephalin (leu-enkephalin), we observed enkephalin localization consistent with data that have previously been reported in the rat, with notable exceptions including lateral septum, ventromedial nucleus of the hypothalamus and cingulate gyrus. Additionally, met- and leu-enkephalin localization patterns largely overlap. Consistent with the post-translational processing of preproenkephalin, met-enkephalin was more abundant than leu-enkephalin both within individual cells (darker staining), and within given brain nuclei (more met-enkephalin immunoreactive cells). Two exceptions were the posterointermediate bed nucleus of the stria terminalis, containing more neurons heavily labeled for leu-enkephalin, and the main olfactory bulb, where only met-enkephalin was observed. Of most interest for this study was the observation of Enk-ir cells and terminals in areas implicated in both sexual and agonistic behaviors in this species.
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PMID:Distribution of methionine and leucine enkephalin neurons within the social behavior circuitry of the male Syrian hamster brain. 1556 35

G-protein-coupled receptor 135 (GPCR135), a former orphan GPCR also known as SALPR, has recently been shown to be modulated by relaxin-3 (R3). In addition to GPCR135, R3 has been shown to be an agonist for GPCR142 (which is a pseudogene in the rat) and to activate LGR7, which is primarily the receptor for relaxin-1/2. The interaction of R3 with LGR7 has confounded the autoradiographic study of the GPCR135 distribution in the rat CNS due to significant expression of LGR7 in the brain. R3/I5, a chimera of the B-chain of R3 bonded to the A-chain of INSL-5, is a specific GPCR135 agonist which is highly selective for GPCR135 over LGR7. [(125)I]R3/I5 specifically binds to sites on rat brain sections with a pharmacology matching results from membrane preparations of recombinant GPCR135 receptors. Autoradiographic studies show the GPCR135 receptor density is most prominent in areas such as the olfactory bulb, sensory cortex, amygdala, thalamus, paraventricular nucleus, supraoptic nucleus, inferior and superior colliculus. The GPCR135 mRNA distribution generally overlaps the pattern of GPCR135 binding sites shown by autoradiography using [(125)I]R3/I5. The nucleus incertus, which has been implicated in the extrapituitary actions of corticotropin-releasing hormone, is the primary source of R3 in the rat central nervous system and expresses GPCR135 receptors. These binding autoradiography and in situ hybridization data suggest that GPCR135 plays an important role in the central processing of sensory signals in rats, are consistent with a putative role for R3/GPCR135 as modulators of stress responses, and confirm the identity of R3 as the central nervous system ligand for GPCR135.
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PMID:Distribution of G-protein-coupled receptor (GPCR)135 binding sites and receptor mRNA in the rat brain suggests a role for relaxin-3 in neuroendocrine and sensory processing. 1567 80

In the present study, we examined the anxiolytic and antidepressant effects of MCL0042, a novel compound showing activity in both MC4 receptor antagonism and serotonin transporter inhibition. MCL0042 showed relatively high affinity for the MC4 receptor and serotonin reuptake site, as determined by receptor binding assays. MCL0042 attenuated [Nle(4),d-Phe(7)]alpha-MSH-increased cAMP formation in MC4 receptor expressing cells, and it inhibited [(3)H]serotonin uptake by rat brain synaptosomes; thus, MCL0042 is an MC4 receptor antagonist and serotonin transporter inhibitor. Subcutaneous administration of MCL0042 significantly increased the number of licks in a Vogel punished drinking test in rats, and it also significantly attenuated swim stress-induced reduction in time spent in open arms in an elevated plus-maze task in rats, showing the anxiolytic-like potential of MCL0042. Moreover, repeated administration of MCL0042 for 14 days attenuated olfactory bulbectomy-induced locomotor hyperactivity in rats, indicating antidepressant-like potential. These data show that MCL0042 has unique properties of both the MC4 receptor antagonist and serotonin transporter inhibitor, and produces anxiolytic and antidepressant activity in rats. Moreover, blockade of both the MC4 receptor and serotonin reuptake sites might represent a useful approach in the treatment of anxiety and depression.
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PMID:MCL0042: a nonpeptidic MC4 receptor antagonist and serotonin reuptake inhibitor with anxiolytic- and antidepressant-like activity. 1633 61

Endogenous opioid peptides (EOPs) are an important class of modulators of the hypothalamo-pituitary axis; treatment with opiates leads to inhibition of GnRH and LH secretion and suppression of reproductive functions. However, little work has been done to investigate the effect of opiates on the electrical activity of GnRH neurons, which ultimately controls GnRH secretion. The purpose of the present study was to investigate the effects of the EOP beta-endorphin on electrical activity of GnRH neurons located in the terminal nerve (TN) associated with the olfactory bulb. We used an excised intact brain preparation from transgenic medaka in which green fluorescent protein (GFP) is genetically expressed in TN-GnRH neurons. These GFP-expressing neurons were then targeted for whole-cell current clamp recordings. Treatment with beta-endorphin led to changes in several characteristics of electrical activity, including depolarization of membrane potential and a decrease in spike amplitude--similar to that observed in response to depolarizing high K(+) treatment. This finding suggests a model in which beta-endorphin depolarizes membrane potential leading to Na(+)-channel inactivation, and subsequent suppression of action-potential amplitude. On the other hand, beta-endorphin had no effect on membrane potential in synaptically isolated GnRH neurons. These results suggest that beta-endorphin is acting indirectly on TN-GnRH neurons to inhibit action potential firing.
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PMID:Beta-endorphin alters electrical activity of gonadotropin releasing hormone neurons located in the terminal nerve of the teleost medaka (Oryzias latipes). 1691 75

In Xenopus laevis, corticotrophin-releasing factor (CRF) and urocortin 1 are present in the brain and they both are potent stimulators of alpha-melanophore stimulating hormone (MSH) secretion by melanotroph cells in the pituitary gland. Because both CRF and urocortin 1 bind with high affinity to CRF receptor type 1 (CRF1) in mammals and Xenopus laevis, one of the purposes of the present study was to identify the sites of action of CRF and urocortin 1 in the Xenopus brain and pituitary gland. Moreover, we raised the hypothesis that the external light intensity is a physiological condition controlling CRF1 expression in the pituitary melanotroph cells. By in situ hybridisation, the presence of CRF1 mRNA is demonstrated in the olfactory bulb, amygdala, nucleus accumbens, preoptic area, ventral habenular nuclei, ventromedial thalamic area, suprachiasmatic nucleus, ventral hypothalamic area, posterior tuberculum, tectum mesencephali and cerebellum. In the pituitary gland, CRF1 mRNA occurs in the intermediate and distal lobe. The optical density of the CRF1 mRNA hybridisation signal in the intermediate lobe of the pituitary gland is 59.4% stronger in white-adapted animals than in black-adapted ones, supporting the hypothesis that the environmental light condition controls CRF1 mRNA expression in melanotroph cells of X. laevis, a mechanism likely to be responsible for CRF- and/or urocortin 1-stimulated secretion of alpha-MSH.
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PMID:Localisation and physiological regulation of corticotrophin-releasing factor receptor 1 mRNA in the Xenopus laevis brain and pituitary gland. 1696 98

Olfactory neuroblastomas are rare, slow-growing malignant tumors, usually diagnosed at advanced stages. Ectopic adrenocorticotropic hormone (ACTH) syndrome caused by an olfactory neuroblastoma is extremely rare. We reported two Korean women who suffered from ectopic ACTH syndrome (EAS) caused by olfactory neuroblastomas. The first patient was a 66-year-old woman who had been diagnosed as olfactory neuroblastoma and refused the management two years before and the second patient was a 37-year-old woman on chemotherapy for olfactory neuroblastoma. In the first case, she presented the Cushingoid appearance with systemic edema and her tumor was removed surgically. ACTH secretion by the tissue was confirmed by immunohistochemistry. By contrast, the second patient presented as severe pneumonia caused by cytomegalovirus and was treated with anti-viral agent followed by chemotherapy and radiotherapy, and her residual mass remained. However, after treatment, both patients' plasma ACTH and cortisol levels returned to normal without any adrenolytic therapy. Considering the causative tumors of EAS can be rarely cured and EAS increases the susceptibility to infections, it is prudent to suppress any hypercortisolemia initially, apart from treating the causal malignancy.
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PMID:Two cases of ectopic adrenocorticotropic hormone syndrome with olfactory neuroblastoma and literature review. 1846 86

Wistar rats strain with passive strategy of the adaptive behavior were selected in T-maze labyrinth. The rats were exposed to water-immerssions stress and after 10 days from their brain the olfactory cortex slices were prepared. The evoked focal potentials were registered in slices. It is shown that the amplitudes of the AMPA and NMDA EPSPs were reduced as compared to control (rats without stress). The amplitude of the GABABergic inhibitory postsynaptic potentiation was increased after stress. Additions of the corticotropin-releasing hormone (10(-10) M) in incubation medium result in reversible inhibition of synaptic transmission. Tetanic stimulation of the slices induced of the long-term posttetanic depression in 84 % slices and in 12 %--to the long-term posttetanic potentiation. It is indicates that the significant disturbances in synaptic transmission in slices. Thus the activation of the corticotrophinergic mechanisms in cortical structures not promots the removal of the rats depressive state with passive strategy of the adaptive behavior induced by inescapable stress.
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PMID:[Electrophysiological characteristics of depressive conditions with passive strategy of the adaptive behavior in rats]. 1851 55

Ecto-nucleotide pyrophosphatases/phosphodiesterases (E-NPPs) are membrane-bound ecto-enzymes involved in the modulation of purinergic signaling. Important physiological roles related to brain development have been associated to purinergic neurotransmission. NPP1, two splice isoforms of NPP2, and NPP3 have already been identified in adult rat brain. However, there are no studies evaluating the mRNA expression of these NPP members during the brain development. The effort of the present study was to map NPP gene expression pattern in olfactory bulb, hippocampus, cerebral cortex, striatum, and cerebellum at crucial ages for rat development (7, 14, 21, 60, and 150 days old) by a semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) strategy. Our results demonstrated an increase in the relative expression of NPP1 throughout the aging in all structures analyzed, except in hippocampus, where the higher expression has been detected in 14 days old rats. Both NPP2 isoforms have shown a similar pattern of expression among all structures. The relative expression of NPP3 decreased during the aging mainly on cerebellum, hippocampus, and olfactory bulb. Altogether, the different patterns of NPP gene expression during rat brain development reinforce the idea that each enzyme may play a distinct role on modulating the purinergic signaling throughout aging.
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PMID:Expression mapping of ectonucleotide pyrophosphatase/phosphodiesterase 1-3 (E-NPP1-3) in different brain structures during rat development. 1856 16

Urocortin 3 (UCN3) is strongly expressed in specific nuclei of the rodent brain, at sites distinct from those expressing urocortin 1 and urocortin 2, the other endogenous ligands of corticotropin-releasing hormone receptor type 2 (CRH-R2). To determine the physiological role of UCN3, we generated UCN3-deficient mice, in which the UCN3 open reading frame was replaced by a tau-lacZ reporter gene. By means of this reporter gene, the nucleus parabrachialis and the premammillary nucleus were identified as previously unknown sites of UCN3 expression. Additionally, the introduced reporter gene enabled the visualization of axonal projections of UCN3-expressing neurons from the superior paraolivary nucleus to the inferior colliculus and from the posterodorsal part of the medial amygdala to the principal nucleus of the bed nucleus of the stria terminalis, respectively. The examination of tau-lacZ reporter gene activity throughout the brain underscored a predominant expression of UCN3 in nuclei functionally connected to the accessory olfactory system. Male and female mice were comprehensively phenotyped but none of the applied tests provided indications for a role of UCN3 in the context of hypothalamic-pituitary-adrenocortical axis regulation, anxiety- or depression-related behavior. However, inspired by the prevalent expression throughout the accessory olfactory system, we identified alterations in social discrimination abilities of male and female UCN3 knock-out mice that were also present in male CRH-R2 knock-out mice. In conclusion, our results suggest a novel role for UCN3 and CRH-R2 related to the processing of social cues and to the establishment of social memories.
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PMID:Urocortin 3 modulates social discrimination abilities via corticotropin-releasing hormone receptor type 2. 2061 Jul 44


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