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)

We studied by immunohistochemistry the distribution of differentiation-associated sodium-dependent inorganic phosphate (Pi) cotransporter (DNPI) in the rat forebrain, in comparison with brain-specific cotransporter (BNPI). DNPI-staining was principally seen in axonal synaptic terminals which showed a widespread but discrete pattern of distribution different from that of the BNPI-staining. In the diencephalon, marked DNPI-staining was seen in the dorsal lateral geniculate, medial geniculate, ventral posterolateral, ventral posteromedial, anterior, and reticular thalamic nuclei without the colocalization with BNPI-staining. DNPI-staining showed a strong mosaical pattern and overlapped well the BNPI-staining in the medial habenular nucleus. DNPI-staining was moderate over the hypothalamus and notably localized in neurosecretory terminals containing corticotropin-releasing hormone in the median eminence. In contrast, the BNPI-staining was region-related and strong in the ventromedial and mammillary nuclei. In the telencephalon, laminar DNPI-staining was seen over the neocortex, corresponding to the thalamocortical termination, and also found in the retrosplenial cortex and the striatum, with the highest intensity in the accumbens nucleus shell. The present results suggest that DNPI serves as a dominant Pi transport system in synaptic terminals of diencephalic neurons including thalamocortical and thalamostriatal pathways as well as the hypothalamic neuroendocrine system in the rat forebrain.
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PMID:Differential localization and colocalization of two neuron-types of sodium-dependent inorganic phosphate cotransporters in rat forebrain. 1138 7

After synaptic release, glutamate is taken up by the nerve terminal via a plasma membrane-associated protein termed excitatory amino acid transporter 3 (EAAT3). Following entry into the nerve terminal, glutamate is pumped into synaptic vesicles by a vesicular transport system. Three different vesicular glutamate transporter proteins (VGLUT1-3) representing unique markers for glutamatergic neurons were recently characterized. The presence of EAAT3, glutaminase and VGLUT1-3 was examined in mouse, rat and rabbit species at mRNA and protein levels in hypothalamic neurons which are involved in the regulation of body weight using in situ hybridization and immunohistochemistry. EAAT3 and glutaminase mRNAs were demonstrated in all parts of the arcuate nucleus in the dorsomedial and ventromedial hypothalamic nuclei and lateral hypothalamic area. VGLUT1 mRNA was present in the magnocellular lateral hypothalamic nucleus. VGLUT2 mRNA was demonstrated in a subpopulation of neurons in the arcuate nucleus and in the ventromedial and dorsomedial hypothalamic nuclei and lateral hypothalamic area. Few VGLUT3 mRNA expressing neurons were scattered throughout the medial and lateral hypothalamus. EAAT3-like immunoreactivity (-li) was demonstrated in glutamate, neuropeptide Y (NPY), agouti-related peptide (AGRP), pro-opiomelanocortin (POMC), cocaine and amphetamine-regulated transcript (CART), melanin-concentrating hormone and orexin-immunoreactive (-ir) neurons. VGLUT2-li could only be demonstrated in POMC- and CART-ir neurons of the ventrolateral arcuate nucleus. The results show that key neurons involved in regulation of energy balance are glutamatergic and/or densely innervated by glutamatergic nerve terminals. Whereas orexigenic NPY/AGRP neurons situated in the ventromedial part of the arcuate nucleus are mainly GABAergic, it is shown that several anorexigenic POMC/CART neurons of the ventromedial arcuate nucleus are most likely glutamatergic [corrected].
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PMID:Plasma membrane and vesicular glutamate transporter mRNAs/proteins in hypothalamic neurons that regulate body weight. 1295 25

Glutamate plays a role in the central regulation of the hypothalamic-pituitary-adrenal (HPA) and thyroid (HPT) axes. Until the recent discovery of vesicular glutamate transporters (VGLUT1-3), there was no specific tool for the examination of the putative morphological relationship between the glutamatergic and the hypophysiotropic systems. Using antisera against VGLUT2, corticotropin-releasing hormone (CRH), and prothyrotropin-releasing hormone (proTRH) (178-199), we performed double-labeling immunocytochemistry at light and electron microscopic levels in order to study the glutamatergic innervation of the CRH- and TRH-synthesizing neurons in the hypothalamic paraventricular nucleus (PVN). Fine VGLUT2-immunoreactive (IR) axons very densely innervated the parvocellular subdivisions of the PVN. VGLUT2-IR axons established juxtapositions with all parvocellular CRH- and TRH-synthesizing neurons. The innervation was similarly intense in all parvocellular subdivisions of the PVN. At ultrastructural level, VGLUT2-IR terminals frequently established synapses with perikarya and dendrites of the CRH- and proTRH-IR neurons. These findings demonstrate that glutamatergic neurons directly innervate hypophysiotropic CRH and TRH neurons in the PVN and, therefore, support the hypothesis that the glutamate-induced activation of the HPA and HPT axes may be accomplished by a direct action of glutamate on hypophysiotropic CRH and TRH systems.
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PMID:Glutamatergic innervation of corticotropin-releasing hormone- and thyrotropin-releasing hormone-synthesizing neurons in the hypothalamic paraventricular nucleus of the rat. 1578 Oct 46

Recent evidence indicates that hypophysiotropic gonadotropin-releasing hormone (GnRH), corticotropin-releasing hormone (CRH) and thyrotropin-releasing hormone (TRH) neurons of the adult male rat express mRNA and immunoreactivity for type-2 vesicular glutamate transporter (VGLUT2), a marker for glutamatergic neuronal phenotype. In the present study, we investigated the issue of whether these glutamatergic features are shared by growth hormone-releasing hormone (GHRH) neurons of the hypothalamic arcuate nucleus (ARH) and somatostatin (SS) neurons of the anterior periventricular nucleus (PVa), the two parvicellular neurosecretory systems that regulate anterior pituitary somatotrophs. Dual-label in situ hybridization studies revealed relatively few cells that expressed VGLUT2 mRNA in the ARH; the GHRH neurons were devoid of VGLUT2 hybridization signal. In contrast, VGLUT2 mRNA was expressed abundantly in the PVa; virtually all (97.5 +/- 0.4%) SS neurons showed labelling for VGLUT2 mRNA. In accordance with these hybridization results, dual-label immunofluorescent studies followed by confocal laser microscopic analysis of the median eminence established the absence of VGLUT2 immunoreactivity in GHRH terminals and its presence in many neurosecretory SS terminals. The GHRH terminals, in turn, were immunoreactive for the vesicular gamma-aminobutyric acid (GABA) transporter, used in these studies as a marker for GABA-ergic neuronal phenotype. Together, these results suggest the paradoxic cosecretion of the excitatory amino acid neurotransmitter glutamate with the inhibitory peptide SS and the cosecretion of the inhibitory amino acid neurotransmitter GABA with the stimulatory peptide GHRH. The mechanisms of action of intrinsic amino acids in hypophysiotropic neurosecretory systems require clarification.
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PMID:Presence of vesicular glutamate transporter-2 in hypophysiotropic somatostatin but not growth hormone-releasing hormone neurons of the male rat. 1586 8

Pro-opiomelanocortin (POMC) and agouti-related protein (AGRP) neurons in the hypothalamus regulate various aspects of energy homeostasis and metabolism. POMC and AGRP neurons, respectively, agonize and antagonize melanocortin receptors on their common downstream neurons. However, it is unknown whether they also reciprocally stimulate and inhibit the same neurons by amino acid transmitters. Whereas AGRP neurons are mostly GABAergic, surprisingly, only a small population of POMC neurons has been found to be glutamatergic, and a significantly larger subpopulation to be GABAergic. To further examine amino acid phenotypes of POMC neurons, we studied mRNA expression for the glutamatergic marker, type 2 vesicular glutamate transporter (VGLUT2), and the GABA synthetic enzyme, glutamic acid decarboxylase 67 (GAD67), in POMC neurons of both rats and mice by using in situ hybridization techniques. In rats, approximately 58% of POMC neurons were labeled for VGLUT2 and 37% for GAD67 mRNA. In mice, approximately 43% of POMC neurons contained VGLUT2, and 54% contained GAD67 mRNA. In both species, a prominent mediolateral distribution pattern was observed at rostral and mid levels of the POMC cell group with VGLUT2-POMC neurons dominating in lateral portions and GAD67-POMC neurons in medial portions. These data demonstrate that both glutamatergic and GABAergic cells are present in comparably significant numbers among POMC neurons. Their glutamatergic or GABAergic phenotype may represent a major functional division within the POMC cell group.
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PMID:Distinct glutamatergic and GABAergic subsets of hypothalamic pro-opiomelanocortin neurons revealed by in situ hybridization in male rats and mice. 2364 Jul 96