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 mice carrying the autosomal recessive gene weaver, there is a massive postnatal loss of dopamine in the caudoputamen, the target of the nigrostriatal system, with relative (though not complete) preservation of dopamine in the ventral striatum, a target of the mesolimbic system. There is concomitant death of catecholaminergic neurons in the substantia nigra, with much less cell death in the limbic midbrain area. In the study reported here, we have reexamined the mesostriatal system of weaver mice by means of tyrosine hydroxylase (TH) immunohistochemistry in order to determine the local architecture of the defect within the striatum and substantia nigra. For the dorsal striatum, the most striking finding was the appearance in the weaver caudoputamen of small pockets of especially weak immunostaining within a larger dorsal zone of generally reduced TH-positive neuropil. These pockets were identified as striosomes by calbindin28k and met-enkephalin immunohistochemistry carried out on adjacent sections. In dorsal, central, and caudal sectors of the caudoputamen, there was also more generalized depletion of TH-immunoreactive neuropil. In the mid-brains of the mutants, the patterns of loss of TH-positive neurons appeared to correspond to these distributions of reduced immunostaining in the striatum. In the substantia nigra pars compacta, ventrally situated TH-positive neurons were especially affected, suggesting preferential depletion of TH-positive neurons projecting to striosomes. In addition, there was a central sector of nearly complete loss of TH-positive neurons in the substantia nigra para compacta and a marked depletion of TH-positive neurons in cell group A8 that, together, may have accounted for the diminution of TH-positive innervation of the striatal matrix. We conclude that the effects of the weaver gene discriminate among mesostriatal subsystems not only according to the regional affiliations of these subsystems within the dorsal and ventral striatum, but also according to the preferential association of the subsystems for the striosomal and matrical compartments of the caudoputamen. The depletion of TH-positive innervation was not confined to the dorsal striatum proper. The defect extended into the adjoining nucleus accumbens, where it appeared to affect the lateral "core" division, and included also a lateral part of the olfactory tubercle. Thus, as in the dorsal striatum, the defect in the TH-positive innervation of the ventral striatum closely follows the local architecture of this striatal region. Neuronal loss in the ventral tegmental area was not evident on qualitative analysis, but at the border between lateral cell group A 10 and medial cell group A9 there was obvious loss of immunostained neurons.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Patterns of cell and fiber vulnerability in the mesostriatal system of the mutant mouse weaver. I. Gradients and compartments. 169 Jul 89

After the recent demonstration of the facilitatory effect exerted by corticotropin-like intermediate lobe peptide (CLIP or adrenocorticotropic hormone (ACTH) 18-39) on paradoxical sleep in the rat (Chastrette and Cespuglio, 1985), we undertook the production of monoclonal antibodies against this peptide. Wistar rats were immunized against CLIP and their spleen cells fused with mouse myeloma cells. After recloning, 25 supernatants were found to give positive immunohistochemical reactions in the rat brain. In immunohistochemical tests performed by preabsorption, the 25 supernatants presented similar properties, i.e. recognized CLIP, ACTH (1-39) and ACTH (25-39), but not ACTH (1-24) and the C-terminal fragment (34-39). We assume that the epitope(s) recognized by the 25 supernatants is (are) located between the amino-acids Asn25 and Ala34 of the CLIP molecule. The immunoreactivity observed in the rat brain and hypophysis with this antibody was distributed with a pattern quite similar to that described for anti-ACTH antibodies. A main group of immunoreactive cell bodies was located in the mediobasal hypothalamus and a small group in the nucleus of the solitary tract. Immunoreactive fibres were distributed from the olfactory nucleus to the spinal cord and formed particularly rich networks in the hypothalamus and preoptic area. Among other locations, immunoreactive axons were also present in the brainstem centres involved in the control of the sleep-waking cycle, which is in accordance with the influence of CLIP on paradoxical sleep. Using Abercrombie's formula, the number of immunoreactive cells in the mediobasal hypothalamus was estimated at about 3000 neurons. We conclude that our monoclonal anti-CLIP antibody can be considered as a good marker of proopiomelanocortin neurons.
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PMID:A monoclonal antibody directed against CLIP (ACTH 18-39). Anatomical distribution of immunoreactivity in the rat brain and hypophysis with quantification of the hypothalamic cell group. 216 15

The distribution of proopiomelanocortin (POMC)-immunoreactive neurons was examined in the forebrains of nine sexually mature female pigs by indirect biotin-avidin horseradish peroxidase immunocytochemistry. Primary antiserum against ovine beta-endorphin (Bioflex #BF-EP-3-1) yielded positive staining of neuronal perikarya and processes. Adjacent control sections treated either with primary antiserum preabsorbed with beta-endorphin or substituted with normal rabbit serum lacked specific staining. POMC-immunoreactive cells were located in the anterior and intermediate lobe of the pituitary gland. POMC-immunoreactive perikarya were located in the arcuate nucleus and periarcuate area. The pituitary stalk/median eminence contained sparsely distributed POMC-immunoreactive fibers, which were confined to the zona interna. POMC-immunoreactive fibers were located in the arcuate nucleus and extended rostrally from the arcuate nucleus into the telencephalon coursing adjacent to the wall of the third ventricle as well as through the anterior hypothalamus, suprachiasmatic, supraoptic nuclei and preoptic areas to the nucleus accumbens, diagonal band of Broca, olfactory tubercle, bed nucleus of the stria terminalis and the ventro-lateral aspect of the septum. Caudal projections extended along the wall of the third ventricle to the level of the mammillary bodies and also coursed dorsally, passing through the periventricular, paraventricular, and dorsal medial nuclei of the hypothalamus to the midline thalamic nuclei and habenular nucleus. Lateral projections extended from the arcuate nucleus along the dorsal aspect of the optic tract and terminated in the amygdaloid complex. The distribution of POMC-immunoreactive perikarya and fibers is similar to that of the luteinizing hormone-releasing hormone (LHRH) fiber network. Therefore the opportunities exist, anatomically, for interactions between the POMC and the LHRH systems.
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PMID:Localization of proopiomelanocortin (POMC) immunoreactive neurons in the forebrain of the pig. 252 70

The localization and distribution of prolactin-like-immunoreactive perikarya and nerve fibers in the rat central nervous system have been studied by a preembedding immunoperoxidase method using well-characterized specific immunsera to rat prolactin. Although the localization of labeled neuronal structures in a number of brain areas correlates with the data of previous immunocytochemical studies, we found prolactin-immunoreactive neurons in various regions not previously reported. In untreated animals, the highest concentrations of prolactin-fibers were observed: (i) in the external layers of the median eminence where they exhibited close contact with blood vessels, and (ii) in the bed nucleus of the stria terminalis and in the central nucleus of the amygdala where they closely surrounded unlabeled perikarya. Dense networks of finely varicose prolactin fibers were also observed in the organum vasculosum of the lamina terminalis, in the subfornical organ, and in the dorsolateral regions of the medulla oblongata and the spinal cord. Lastly, a number of large, varicose, intensely immunoreactive fibers were found in the olfactory bulb, the cingulum, and the periventricular regions of the hypothalamus and central gray, whereas isolated fibers could be detected in the caudate nucleus and in the cerebral cortex. In animals treated with colchicine, prolactin-immunoreactive perikarya were essentially located within the periventricular and perifornical regions of the hypothalamus, and within the bed nucleus of the stria terminalis. Although corticotropin (ACTH 17-39)-immunoreactive fibers could be detected in several regions found to contain prolactin fibers, the distribution and organization of both fiber types clearly differed in numerous brain regions, and the regions containing the corresponding perikarya did not overlap.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The organization of prolactin-like-immunoreactive neurons in the rat central nervous system. Light- and electron-microscopic immunocytochemical studies. 254 74

We examined the effects of chronic treatment with antidepressants (imipramine or desipramine) or benzodiazepines (diazepam, alprazolam, or adinazolam) on modulation of corticotropin-releasing-factor (CRF) receptors in discrete areas of rat brain and in anterior pituitary. As previously reported, we found that chronic antidepressant treatment downregulated 5-HT2 serotonin and beta-adrenergic receptors in cerebral cortex. Although there was a trend toward increased CRF binding in brain stem, striatum, cerebellum, hypothalamus, and frontal cerebral cortex following antidepressant treatment, the changes were only statistically significant in brain stem in imipramine-treated rats. In addition, no significant changes were seen in CRF binding in other brain regions including parietal/temporal cerebral cortex, olfactory bulb, hippocampus, and anterior pituitary. Following chronic benzodiazepine treatment CRF receptor binding was significantly decreased in the frontal cerebral cortex and hippocampus; although there was a trend for CRF receptors to be decreased in other brain areas and increased in anterior pituitary, the changes were not statistically significant.
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PMID:Effects of chronic antidepressant and benzodiazepine treatment on corticotropin-releasing-factor receptors in rat brain and pituitary. 255 44

Immunoreactive (IR) prolactin was localized immunocytochemically in cell bodies in the mediobasal hypothalamus and in fibers in many regions of the rat brain. The cell bodies were found in the arcuate nuclei and the adjacent areas ventral to the ventromedial nuclei. Fiber projections extended rostrally to and/or through the anterior hypothalamus, preoptic area, nucleus accumbens, septum, diagonal bands of Broca, caudate-putamen, frontal cortex and accessory olfactory bulb; laterally to the amygdala, especially the central nucleus and some parts of the medial nucleus; caudally to and/or through the midbrain central gray, reticular formation, parabrachial region, and several portions of the lower brain stem and spinal cord extending to sacral levels. The system appears to be essentially identical to that containing proopiomelanocortin (POMC) and its processed peptides, as shown by double immunocytochemistry. Preabsorption of the antiprolactin antiserum with either prolactin or the 16,000-dalton N-terminus of POMC eliminated immunoreactivity in the brain. Preabsorption with other POMC-derived peptides, including beta-lipotropic hormone, beta-endorphin, met-enkephalin, adrenocorticotrophic hormone (1-24), corticotropin-like intermediate lobe peptide, alpha- and gamma-melanocyte-stimulating hormones and an octapeptide region of the N-terminus of POMC bearing some homology with prolactin, did not eliminate immunoreactivity in the brain. Similarly, preabsorption with growth hormone, luteinizing hormone, follicle-stimulating hormone, motilin or fetuin did not eliminate immunoreactivity in the brain. The antiprolactin antiserum also recognized all cells in the intermediate lobe and a subset of cells in the anterior lobe of the Snell dwarf mouse pituitary. This immunoreactivity was eliminated by preabsorption of the antiserum with prolactin or with the 16,000-dalton N-terminus of POMC. These results suggest that IR prolactin in the brain may be related to the N-terminus of POMC. Additional results based on one- and two-dimensional gel electrophoresis and immunoblotting indicate that the antiprolactin antiserum used in the majority of the immunocytochemical studies recognized a number of proteins.
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PMID:Distribution and partial characterization of immunoreactive prolactin in the rat brain. 271 51

The effects of hypothalamic deafferentations and brain lesions on adrenocorticotropin (ACTH) and corticosterone (CS) responses after neural stimuli were studied in rats. It was found that the various modalities are mediated by different neural pathways. Photic and acoustic stimuli utilize a posterior input, whereas the sciatic and olfactory modalities are mediated by anterior afferents and forebrain limbic structures. The effects of limbic extrahypothalamic structures on the hypothalamus are transmitted by both anterior and posterior inputs. The medial forebrain bundle (MFB) was found to have a differential role in the mediation of ACTH and CS responses. To identify the neurotransmitters involved, rats were injected with 6-hydroxydopamine in the MFB and 5,7-dihydroxytryptamine in the raphe nuclei. The depletion of hypothalamic norepinephrine and serotonin caused inhibition of the adrenocortical responses only after photic stimulation, and only of responses to limbic stimuli in the former group. In view of the location of corticotropin-releasing factor in the paraventricular nucleus, responses to afferent stimuli were studied in this region in identified neurons projecting to the median eminence. Stimuli that increased or decreased CS secretion facilitated or inhibited cell firing, respectively, thus demonstrating a possible electrophysiological correlate of neuroendocrine regulation.
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PMID:Neural pathways mediating adrenocortical responses. 285 40

One hundred and two prepubertal pigs were used in two experiments to determine if adrenocorticotropin hormone (ACTH)-induced increase in submissive behavior could be mediated by odorous signals. In experiment one, urine was collected from pigs treated with either 0, 1 or 10 IU/kg ACTH. Urine from pigs given 1.0 IU/kg ACTH caused a trend for a rise in submissive behavior. Level of plasma cortisol from donor pigs correlated well (r = .92) with duration of submissive behavior in the tested pigs. In experiment two, urine from ACTH-treated pigs increased submissive behavior when sprayed in the air during late fight. Thus, ACTH-induced submissiveness may be mediated by a pheromone. These results fit the hypothesis that, in addition to visual cues, an olfactory cue (perhaps adrenal in origin) is released towards the end of a fight to signal submission. Aerosolizing urine from ACTH-treated pigs may have interfered with this pheromonal signal.
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PMID:Olfactory cues and pig agonistic behavior: evidence for a submissive pheromone. 298 88

Light microscopic autoradiography was used to visualize the neuroanatomical distribution of rat brain delta opioid receptors. Slide-mounted sections of rat brain were labeled with [3H]-[2-D-penicillamine, 5-D-penicillamine]enkephalin([3H]DPDPE), a highly selective delta opioid agonist. Saturation isotherms of [3H]DPDPE binding to thaw-mounted brain slices gave a maximal number of binding sites of 79.9 fmol/mg of protein and an apparent dissociation constant (Kd) of 6.3 nM. DPDPE and met-enkephalin inhibited [3H]DPDPE binding with high affinity (lC50 values of 6.3 and 13.8 nM, respectively). Putative mu opioid receptor selective ligands such as morphine sulfate, Tyr-D-Ala-Gly-NMePhe-Gyl-ol and [N-MePhe3, D-Pro4]morphiceptin (PL017) were less potent inhibitors of [3H]DPDPE binding. The rat brain areas containing the highest densities of receptors were the claustrum, basolateral amygdaloid nucleus, the caudate-putamen and nucleus accumbens, the external plexiform layer of the olfactory bulb and the olfactory tubercle. Moderate receptor density was characteristic of the hippocampal formation in which grains were seen over the molecular layer of the dentate gyrus and stratum oriens (CA1), and of the different layers of cerebral cortex. Generally, low density of binding was found over the thalamus and the septal nuclei. Low specific binding was also seen in the cerebellum, medulla oblongata and in the dorsal horn of the spinal cord. There was little specific [3H]DPDPE binding over the white matter areas.
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PMID:Light microscopic autoradiographic localization of delta opioid receptors in the rat brain using a highly selective bis-penicillamine cyclic enkephalin analog. 301 47

Opioid peptides, particularly beta-endorphin, methionine- (MEK) and leucine-enkephalin, and dynorphin, are involved in the regulation of food intake in mammals. The precursor molecules of these peptides undergo differential processing in brain areas producing regional concentration differences in opioids. Intraregional concentration changes also accompany alterations in feeding states. For example, MEK concentrations decrease in the basomedial hypothalamus, amygdala, and olfactory bulb in fed sheep compared with fasted sheep. Moreover, these changes are species specific. In sheep, beta-endorphin decreases in the dorsomedial and posterior hypothalami after feeding, but in the rat it is increased in the ventromedial hypothalamus and decreased in the posterior hypothalamus. In addition, immunohistochemical localization of cell bodies shows interspecies differences in concentrations. For example, dynorphin is found predominantly in the suprachiasmatic area in sheep, but in the paraventricular nucleus in the rat. These observations indicate that regulation of food intake may be differentially controlled in these species. In sheep, kappa agonists increase food intake, whereas stimulation of delta receptors inhibits feeding. Further clarification of the receptors involved in food intake will necessitate studies with more specific agonists.
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PMID:Opioid peptides and the control of feeding in sheep. 302 55


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