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 man, discrete neurons of the infundibular (arcuate) nucleus contain compounds that can be stained with anti-endorphin (alpha and beta), anti-ACTH, anti-MSH (alpha and beta) and anti-beta-LPH immune sera (I.S.). In the fetus, certain neurons stain with anti-beta-endorphin or anti((17--39)ACTH starting from the 11th week of fetal life. At the ultrastructural level, these neurons contain elementary granules that are immunoreactive with anti-beta-endorphin. In the adult, neurons immunoreactive with anti-beta-endorphin are found in the infundibular nucleus. Their axonal fibers terminate around blood vessels in the neurovascular zone and in the pituitary stalk, or establish contacts with non-immunoreactive perikarya of the infundibular nucleus. These neurons can be stained with anti(17--39)ACTH and anti-beta-endorphin I.S. The most reactive are also stained moderately with anti-alpha-MSH, anti-beta-MSH, anti-beta-LPH, anti-alpha-endorphin, or anti(1--24)ACTH I.S. These results indicate that, in man, compound(s) identical with or immunologically related to endorphins, beta-LPH, ACTH and MSH are secreted by certain hypothalamic neurons. These agents probably originate from a common precursor molecula similar to the so-called pro-opiocortin.
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PMID:Infundibular neurons of the human hypothalamus simultaneously reactive with antisera against endorphins, ACTH, MSH and beta-LPH. 22 33

The distribution and concentration of alpha-MSH in the rodent brain has been determined by radioimmunoassay. The limbic system contained substantial quantities of alpha-MSH. Forty per cent of the alpha-MSH present in the brain was localized in the hypothalamus, with the highest concentration of alpha-MSH in the arcuate nucleus. More than 40% of the extrahypothalamic alpha-MSH in the brain was found in the following areas: midbrain (16%), preoptic area (13%), septum (7%), and thalamus (7%). To determine the source of the hypothalamic and extrahypothalamic alpha-MSH, the anterior hypothalamic preoptic area of the brain was surgically separated from more caudal diencephalic structures, and the arcuate region of the hypothalamus was surgically isolated from the remainder of the brain. Following these deafferentations, no significant reduction in hypothalamic alpha-MSH levels was observed; however, a significant reduction in extrahypothalamic alpha-MSH level was demonstrated. This dramatic decrease of alpha-MSH in extrahypothalamic areas of the rodent brain strongly suggests that the bulk of the extrahypothalamic alpha-MSH arises from neuronal perikarya in the arcuate region. These findings are consistent with the hypothesis that a population of neuronal cell bodies producing alpha-MSH originate in the arcuate region of the hypothalamus and that they send axonal projections to many areas of the limbic system and brain stem.
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PMID:Distribution of alpha-melanocyte-stimulating hormone in the rat brain: evidence that alpha-MSH-containing cells in the arcuate region send projections to extrahypothalamic areas. 49 64

Increasingly strong evidence suggests that cholinergic neurons in the mesopontine tegmentum play important roles in the control of wakefulness and sleep. To understand better how the activity of these neurons is regulated, the potential afferent connections of the laterodorsal (LDT) and pedunculopontine tegmental nuclei (PPT) were investigated in the rat. This was accomplished by using retrograde and anterograde axonal transport methods and NADPH-diaphorase histochemistry. Immunohistochemistry was also used to identify the transmitter content of some of the retrogradely identified afferents. Following injections of the retrograde tracer wheatgerm agglutinin-conjugated horseradish peroxidase (WGA-HRP) into either the LDT or the PPT, labelled neurons were seen in a number of limbic forebrain structures. The medial prefrontal cortex and lateral habenula contained more retrogradely labelled neurons from the LDT, whereas in the bed nucleus of the stria terminalis and central nucleus of the amygdala, more cells were labelled from the PPT. Moderate numbers of neurons were seen in the magnocellular regions of the basal forebrain, and many labelled neurons were observed in the lateral hypothalamus, the zona incerta, and the midbrain central gray from both the LDT and the PPT. Accessory oculomotor nuclei in the midbrain as well as eye movement-related structures in the lower brainstem contained some neurons labelled from the LDT, and fewer neurons from the PPT. A few labelled neurons were seen in somatosensory and other sensory relay nuclei in the brainstem and the spinal cord. Retrograde labelling was seen in a number of extrapyramidal structures, including the globus pallidus, entopenduncular and subthalamic nuclei, and substantia nigra following PPT injections; with LDT injections, labelling was similar in density in the substantia nigra but virtually absent in the entopeduncular and subthalamic nuclei. Data with the fluorescent retrograde tracer fluorogold combined with immunofluorescence indicated that many neurons in the zona incerta-lateral hypothalamic region that were retrogradely labelled from the LDT contained alpha-melanocyte-stimulating hormone. Numerous neurons were labelled throughout the reticular formation of the brainstem following either LDT or PPT injections. Many neurons retrogradely labelled in the LDT and PPT, the dorsal and median raphe nuclei, and the locus ceruleus contained choline acetyltransferase, serotonin, and tyrosine hydroxylase, respectively. The anterograde tracers WGA-HRP and phaseolus vulgaris leucoagglutinin were used to confirm some of the projections indicated by the retrograde labelling data; anterograde labelling was seen in the LDT and PPT following injections of one of these tracers into the medial prefrontal cortex, lateral hypothalamus, and the contralateral LDT.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Afferent connections of the laterodorsal and the pedunculopontine tegmental nuclei in the rat: a retro- and antero-grade transport and immunohistochemical study. 128 Nov 70

The role of alpha 1-adrenergic receptors in the secretion of corticotropin-releasing hormone (CRH) during stress was studied by immunohistochemical analysis of the CRH content of the median eminence (ME) after intracerebroventricular (icv) administration of the alpha 1-adrenergic agonist, methoxamine, or the antagonist, prazosin, in rats pretreated with colchicine. Immunohistochemical staining was performed by the peroxidase technique on 40 microns free-floating sections using a polyclonal antibody specific for CRH. In the first experimental model, rats were implanted with icv cannulae and adapted to the experimental conditions by daily handling and icv injection of artificial CSF. Colchicine (75 micrograms) was administered through the cannulae 6 h before the experiment, conditions in which axonal transport was blocked with little change in basal immunostaining. Two hours after immobilization stress or a single injection of methoxamine (100 micrograms, icv), there was a marked decrease in CRH immunoreactivity throughout the ME, reflecting release of the neuropeptide into the portal circulation. The decrease in CRH immunostaining following immobilization was largely prevented by icv injection of the alpha 1-adrenergic antagonist, prazosin. In the second experimental model, rats were sacrificed 48 h after icv colchicine injection, conditions in which colchicine acts as a stressor and causes marked depletion of irCRH from the ME. This chronic effect of colchicine was also partially prevented by administration of prazosin, 400-ng injection 5 min prior to colchicine, followed by a continuous icv mini-pump infusion of prazosin, indicating that alpha 1-adrenergic stimulation contributes to the action of colchicine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Participation of alpha 1-adrenergic receptors in the secretion of hypothalamic corticotropin-releasing hormone during stress. 132 15

The sites of origin of alpha-melanocyte-stimulating hormone (alpha-MSH)-containing axonal components in the lateral area of the midbrain periaqueductal gray (PAG) were studied in the rat by the retrograde tracing method of horseradish peroxidase, combined with the immunocytochemical technique. The results indicated that alpha-MSH-containing axonal components in the PAG arose not only from the arcuate nucleus of the hypothalamus but also from the ventral zona incerta, the periventricular, perifornical and lateral hypothalamic regions.
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PMID:The sites of origin of a-melanocyte-stimulating hormone-containing axonal components in the lateral area of the midbrain periaqueductal gray of the rat. 157 91

A fairly high number of neuropeptide Y (NPY) and adrenocorticotropic hormone (ACTH) immunoreactive (ir) neuronal perikarya and dense networks of NPY-ir fibers are present in the hypothalamic arcuate nucleus of rats. Light and electron microscopic double immunolabeling techniques were used to demonstrate morphological connections between NPY-ir nerve fibers and ACTH-ir neurons here. Silver-gold intensified diaminobenzidine (DAB) labeling of perikaryal-dendritic immunoreactivity followed by a second, non-intensified DAB chromogen labeling of immunoreactive nerve terminals was used and recommended in the above sequence as a method of choice for the detection of synaptic contacts with double-labeling technique. By this way, NPY-immunoreactivity was localized in axons and axonal terminals forming a variety of conventional synaptic contacts with ACTH-ir neuronal perikarya and dendrites in the arcuate nucleus.
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PMID:Neuropeptide Y innervation of ACTH-immunoreactive neurons in the arcuate nucleus of rats: a correlated light and electron microscopic double immunolabeling study. 215 82

Intraperitoneal administration of human recombinant interleukin-1 (IL-1) to rats can increase blood levels of corticosterone and adrenocorticotropic hormone (ACTH). The route by which IL-1 affects pituitary-adrenal activity is unknown. That the IL-1-induced pituitary-adrenal activation involves an increased secretion of corticotropin-releasing factor (CRF) is indicated by three lines of evidence. First, immunoneutralization of CRF markedly attenuated the IL-1-induced increase of ACTH blood levels. Second, after blockade of fast axonal transport in hypothalamic neurons by colchicine, IL-1 administration decreased the CRF immunostaining in the median eminence, indicating an enhanced release of CRF in response to IL-1. Third, IL-1 did not stimulate ACTH release from primary cultures of anterior pituitary cells. These data further support the notion of the existence of an immunoregulatory feedback circuit between the immune system and the brain.
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PMID:Corticotropin-releasing factor-producing neurons in the rat activated by interleukin-1. 244 79

Pituitary adenomas from 15 patients with Cushing's disease were studied histopathologically. The tumors were examined for the presence of neural axons by the Bodian silver impregnation technique and a specific immunohistologic technique based on a monoclonal antibody to axonal neurofilaments. Axons were not seen in any of the surgical specimens. This finding suggests that most, if not all, adrenocorticotropin-secreting pituitary adenomas are of anterior lobe origin.
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PMID:Pituitary adenomas in Cushing's disease: do they arise from the intermediate lobe? 245 24

The amygdala, particularly the central amygdaloid nucleus, is important for the expression of adrenocorticotropin and corticosterone responses during stress. The aim of the present study was to determine if the central amygdaloid nucleus directly innervated the hypothalamic paraventricular nucleus. To accomplish this aim, the Phaseolus vulgaris leucoagglutinin lectin anterograde tracing method was used. Injections of the tracer into the medial central amygdaloid nucleus resulted in axonal and terminal labeling within the medial and lateral parvocellular parts of the caudal paraventricular nucleus. A dense patch of labeling was observed within the lateral wing of the lateral part of the parvocellular paraventricular nucleus. Only a few labeled axons were observed within the paraventricular nucleus of animals that had lectin injections localized to the lateral part of the central nucleus. Tracer injections localized to the medial amygdaloid nucleus resulted in axonal and terminal labeling primarily within the anterior parvocellular and periventricular regions of the paraventricular hypothalamic nucleus. Sparse to moderate axonal and terminal labeling was observed within the magnocellular parts of the paraventricular nucleus in animals that had injections of tracer into either the medial central nucleus or the medial nucleus. No labeling was observed within the paraventricular nucleus of animals that had injections of lectin within other amygdaloid nuclei or adjacent regions of the striatum. The results demonstrated a topographically organized projection from the amygdala to the hypothalamic paraventricular nucleus. The central nucleus mainly innervates the caudal lateral and medial parvocellular paraventricular nucleus. The medial nucleus innervates the rostral parvocellular parts of the paraventricular nucleus. These pathways could form the anatomical substrates of amygdaloid modulation of neuroendocrine responses to stressors.
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PMID:Direct projections from the central amygdaloid nucleus to the hypothalamic paraventricular nucleus: possible role in stress-induced adrenocorticotropin release. 255 78

An immunocytochemical method was used to reveal beta-endorphin and alpha-melanotropin peptides in nerve profiles at the neuromuscular junctions in the soleus and extensor digitorum longus muscles of the adult rat. After unilateral section of the sciatic nerve, the proportion of endplates with immunoreactive nerve profiles increased in the denervated muscles even after the axonal material in the distal nerve segments had degenerated. When the nerve was sectioned in the mid-thigh region the proportion of immunoreactive endplates increased with time up to 24-36 h after the nerve section and then eventually declined. The incidence of immunoreactive nerve profiles also increased in the proximal stump. After unilateral sciatic nerve section there was also an increase in the incidence of immunoreactive endplates in the contralateral muscles. The increases in the contralateral muscles could be detected at an earlier time if the nerve was sectioned closer to the spinal cord. The possibility is discussed that the expression of pro-opiomelanocortin peptides in the motor nerves is tonically suppressed in the normal adult but the inhibition is released after section of the nerve. The findings indicate that a signal is transferred from the site of injury in the transected nerves to the motor nerves of the contralateral limb via a transneuronal mechanism through the spinal cord.
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PMID:Pro-opiomelanocortin-derived peptides in transected and contralateral motor nerves of the rat. 255 53


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