Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The subcellular compartmentalization and axonal transport of oxytocin and vasopressin messenger RNAs have recently been reported in the rat hypothalamo-posthypophyseal system using in situ hybridization. So far, no data are available concerning the intracellular distribution of co-localized peptide transcripts, for example of galanin, which is synthesized in the vasopressinergic magnocellular neurons of the rat and which is up-regulated in these neurons under different conditions, including salt loading and colchicine injection. In the present study, using non-radioactive in situ hybridization and immunohistochemistry at the light and electron microscope levels, preprogalanin messenger RNA and galanin-like immunoreactivity were localized in the hypothalamo-posthypophyseal system. After salt loading, preprogalanin transcripts were found throughout the perikaryal cytoplasm, especially in the peripheral cytoplasm and in the perinuclear area. Since immunohistochemistry also showed galanin-like immunoreactivity preferentially in the perinuclear area of control rats, galanin synthesis may occur mainly in this cytoplasmic domain. Preprogalanin messenger RNA was also clustered in dendrites containing rough endoplasmic reticulum. The use of a new in situ hybridization method involving tyramide signal amplification, based on catalysed reporter deposition, allowed visualization of preprogalanin messenger RNA in axonal projections running through the internal layer of the median eminence after salt loading, but not in control or in colchicine-injected animals. The negative results obtained after colchicine injection indicate that the mechanism of messenger RNA transport may require an intact cytoskeleton. The labelling was found in non-dilated axon segments as well as in a subset of axonal swellings in the rostral aspect of the median eminence, but was restricted to a few swellings in its caudal part, with no labelling in the posterior pituitary. Thus, preprogalanin messenger RNA was segregated in the axons. The functional significance of messenger RNAs' exportation into axons is not known, but our results suggest that this phenomenon may not be limited to the two principal magnocellular hormone messenger RNAs, but may also involve co-existing peptide messenger RNAs.
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PMID:Subcellular localization of preprogalanin messenger RNA in perikarya and axons of hypothalamo-posthypophyseal magnocellular neurons: an in situ hybridization study. 957 92

The aim of the present study was to analyze the neurochemical properties of the centrifugal visual system (CVS) of the quail using an immunohistochemical approach by testing 16 neuropeptides (angiotensin: ANG, bradykinin: BK, cholecystokinin, dynorphin, L and M-enkephalin, beta-endorphin: beta-END, galanin, alpha-neoendorphin, neurokinin A, neuropeptide Y (NPY), ocytocin, somatostatin, substance P, vasopressin, vasoactive intestinal polypeptide) and three neurotransmitters or their synthetic enzymes (choline acetyltransferase: ChAT, tyrosine hydroxylase: TH, serotonin: 5-HT and nitric oxide synthase: NOS, including the histochemical nicotinamide adenine dinucleotide phosphate diaphorase technique). For each substance, the somatic and afferent fiber and terminal labeling was analyzed within the nucleus isthmo-opticus (NIO) and the ectopic area (EA) and compared with that of retinopetal cell bodies labeled retrogradely with RITC following its intraocular injection (double-labeling procedure). The results showed that none of the centrifugal neurons were reactive to any of the substances tested. In contrast, all with the exception of ANG, BK and beta-END, labeled fibers and terminals within the EA and only four (ChAT, 5-HT, NPY and NOS) within the NIO. Possible sources of these immunoreactive fibers terminating in the NIO and EA were investigated by mapping the somatic immunolabeling of the different substances within brainstem regions previously shown by Miceli and other authors to project upon the centrifugal neurons. The data suggests that, besides the rapid retino-tecto-NIO-retinal loop, which facilitates the transfer of meaningful or more relevant information within particular portions of the visual field, the multiple afferent input which stems from various brainstem regions utilizes a wide range of neuroactive substances. Some of these afferent projections upon the centrifugal neurons appear to belong to nonspecific systems which might play a role in modulating the excitability of centrifugal neurons as a function of arousal.
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PMID:An immunohistochemical study of putative neuromodulators and transmitters in the centrifugal visual system of the quail (Coturnix japonica). 971 61

The distribution and regulation of galanin-R1 receptor (GAL-R1-R) mRNA has been studied in the anterior and mid-diencephalon by using in situ hybridization. Moreover, possible colocalization of GAL-R1-R mRNA and prepro-galanin or vasopressin mRNAs has been analyzed at the cellular level using double in situ hybridization methodology. Many nuclei in the hypothalamus expressed GAL-R1-R mRNA, including the paraventricular nucleus (PVN) and the supraoptic nucleus (SON). Strong expression was also seen in the same sections in various areas outside of the diencephalon. The distribution patterns are similar to those described in earlier studies. Double labeling experiments showed GAL-R1-R mRNA in vasopressin neurons in the PVN and SON. Moreover, GAL-R1-R mRNA and prepro-galanin mRNA were colocalized in several hypothalamic nuclei. GAL-R1-R mRNA levels showed a high degree of plasticity. Thus, salt loading resulted in a marked increase in GAL-R1-R mRNA levels in the PVN and SON and a moderate decrease was seen during lactation. In contrast, hypophysectomy caused a decrease in GAL-R1-R mRNA levels. Differential effects of colchicine were recorded with a decrease of GAL-R1-R mRNA in the magnocellular hypothalamic neurons. After salt loading or during lactation, GAL-R1-R mRNA and prepro-galanin mRNA were regulated in parallel, whereas their levels changed in opposite directions after hypophysectomy and colchicine injection. In conclusion, GAL-R1-Rs are present in several hypothalamic nuclei, partly in neurons synthesizing galanin. The receptors are regulated in a specific fashion in the various nuclei, depending on the stimulus applied. The results suggest that the effect of galanin in the hypothalamus partly depends on the state of receptor expression.
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PMID:Galanin-R1 receptor in anterior and mid-hypothalamus: distribution and regulation. 973 81

The aim of the present study was to verify the hypothesis that stress exposure modifies the content and release of galanin in the hypothalamic paraventricular nucleus and the median eminence. Colchicine and immobilization served as stress stimuli, and the changes in galanin immunoreactivity were compared with those in corticotropin-releasing hormone and vasopressin. In control animals, a limited number of galanin perikarya were identified in the paraventricular nucleus. The high dose (75 microg) of colchicine enhanced galanin in both parvicellular and magnocellular subdivisions, as analysed 72 h later. In the median eminence, galanin accumulated only in the external zone. High-dose colchicine did not affect galanin, while corticotropin-releasing hormone and vasopressin were depleted from the median eminence. Immobilization (120 min) neither alone nor in combination with colchicine influenced galanin immunoreactivity in the external zone. The low dose of colchicine induced an unexpected accumulation of galanin in the internal zone of the median eminence, which was further increased by subsequent immobilization. In the external zone, low-dose colchicine induced a complete disappearance of vasopressin, substantial depletion of corticotropin-releasing hormone and no changes in galanin immunoreactivity. The present studies demonstrate that galanin in the external zone of the median eminence is not influenced by colchicine or by immobilization stress.
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PMID:Stress and colchicine do not induce the release of galanin from the external zone of the median eminence. 979 75

Ca2+ efflux, Ca(2+)-ATPase, and membrane permeability measurements were used to investigate the biochemical mechanisms of Ca2+ release induced by mastoparan (MP) and the chimeric hormone-MP constructs incorporating galanin (galparan) or vasopressin antagonist (M375 and M391) moieties. Comparative studies utilised preparations of porcine cerebellar microsomes and rabbit skeletal muscle sarcoplasmic reticulum (SR). MP and chimeric peptides galparan, M375 and M391 induce Ca2+ release over a range of concentrations from 0.3-10 microM. Comparison of MP and three chimeric, N-terminal extended, constructs indicates that N-terminal extension modifies the biological properties of MP, producing changes in efficacy which are enzyme-isoform-specific. Biochemical studies indicate that the chimeric analogues and MP inhibit Ca(2+)-ATPases and directly activate the ryanodine receptor (RyR) to release Ca2+ from both heavy SR (HSR) and microsomes. The same peptides have no effect on the InsP3 receptor (InsP3R). Other actions that include modest changes in membrane permeability may also contribute to the Ca(2+)-mobilising action of MP and chimeric constructs.
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PMID:Biochemical mechanisms of calcium mobilisation induced by mastoparan and chimeric hormone-mastoparan constructs. 979 86

Evidence suggests that hypothalamic galanin (GAL) has a variety of functions related to energy and nutrient balance, reproduction, water balance, and neuroendocrine regulation. The focus of this chapter is the role of GAL in eating and body weight regulation. Findings described herein demonstrate that GAL, in a cell group of the anterior region of the paraventricular nucleus (aPVN) that projects to the median eminence, has a role in the control of fat intake, fat metabolism, and body fat. This function of aPVN GAL neurons is carried out in close relation to circulating insulin and glucose. Galanin-expressing perikarya in the medial preoptic area (MPOA) have a similar function, although GAL here operates in association with the female steroids estrogen and progesterone. These GAL cell groups of the aPVN and MPOA contrast with those in the arcuate nucleus as well as the magnocellular vasopressin-containing neurons of the PVN and supraoptic nucleus, which show no relation to fat balance. This evidence reveals differential functions for the distinct GAL neuronal cell groups of the hypothalamus.
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PMID:Differential functions of hypothalamic galanin cell grows in the regulation of eating and body weight. 992 72

Galanin and galanin receptors are widely distributed within the central nervous system, but historically much research has been focused on hypothalamic galanin systems including those in the preoptic area, paraventricular nucleus (PVN), supraoptic nucleus (SON), and median eminence. In early studies, galanin mRNA, immunoreactivity, and binding sites were detected in neurons of the SON and both the magnocellular and parvocellular regions of the PVN, all of which also contain vasopressin, oxytocin, and several other peptides. This article briefly reviews some important recent studies of the electrophysiologic effects of galanin on magno-cellular neurons in vitro; regulation of galanin expression by the physiologic stimulus of lactation; the role of parvocellular galanin systems in energy balance, body weight, and obesity; and the regional and cellular localization of galanin and galanin receptor mRNAs in the PVN/SON. In relation to the latter issue, two distinct galanin receptor subtypes, GalR1 and GalR2, have now been cloned and characterized. In situ hybridization histochemical studies of rat brain by several groups have consistently demonstrated GalR1 mRNA in the SON and PVN, in the magnocellular and parvocellular regions. By contrast, our recent experiments using [35S]-labeled oligonucleotide probes detected GalR2 mRNA enriched in the parvocellular, not the magnocellular regions of the PVN, and the transcripts were not detected in the SON, whereas studies by other using a digoxigenin-labeled RNA probe have detected GalR2 mRNA in the SON (and PVN). Nonetheless, given the known effects of hyperosmotic stimuli, changes in metabolic status, and various hormones on galanin synthesis and release and the ability of galanin to regulate the electrical and secretory activity of magnocellular neurons, it will be of interest to determine any possible (differential) regulation of galanin receptor subtype expression and the pre- and postsynaptic roles of GalR1 and GalR2 receptors in magnocellular and parvocellular neurons.
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PMID:Galanin-galanin receptor systems in the hypothalamic paraventricular and supraoptic nuclei. Some recent findings and future challenges. 992 75

Based on early immunocytochemical findings, galanin (GAL) was postulated to function as an inhibitory cotransmitter in rat cholinergic memory pathways. However, recent studies indicate that in the basal state GAL is not widely expressed by forebrain cholinergic neurons in rats. Inhibition of cholinergic transmission by cosecreted GAL may be enhanced under certain conditions, because GAL gene expression in the cholinergic basal forebrain is significantly increased prior to puberty and following nerve growth factor treatment. Other sources of GAL in rat septohippocampus that could interact with cholinergic pathways include noradrenergic neurons in the locus ceruleus and vasopressinergic neurons in the bed nucleus of the stria terminalis (BST) and medial amygdala (Me). GAL is extensively colocalized within these steroid-sensitive cell groups where its expression is upregulated by gonadal hormones. GAL, acting via the GALR1 receptor subtype, does not appear to directly regulate the activity of cholinergic neurons, but it may regulate the release of vasopressin and GAL into septohippocampus from BST/Me neurons.
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PMID:Regulation of galanin in memory pathways. 992 81

Male rats possess twice as many cells that express arginine-vasopressin (AVP) in the bed nucleus of the stria terminalis (BST) and centromedial amygdala (CMA) as do females. This sex difference may arise from sex differences in the induction of AVP expression in galanin (GAL)-expressing cells, which themselves do not differ in number between males and females. To test whether AVP expression could arise from a single pool of galaninergic cells, we determined whether the cell birth profile of GAL-immunoreactive (ir) cells was similar to that of AVP-ir cells. Dams were injected with the cell birth marker bromodeoxyuridine (BrdU) on one of seven gestational dates, ranging from embryonic day 11 (E11) to E17. The resulting offspring were sacrificed at 3 months of age. Processing their brains for the presence of either GAL and BrdU, or AVP and BrdU immunoreactivity revealed that in both the BST and CMA, the majority of GAL-ir and AVP-ir cells were labeled with BrdU on E12 and E13. In contrast, most other cells in the same region were labeled on E14 and E15. The similarity in the timing of cell birth of the GAL-ir and AVP-ir cells is consistent with the idea that GAL-ir cells in the BST/CMA constitute a single pool of cells that may be induced to express AVP during development.
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PMID:Neurogenesis of galanin cells in the bed nucleus of the stria terminalis and centromedial amygdala in rats: a model for sexual differentiation of neuronal phenotype. 1008 84

In golden hamsters, there is a complete absence of the small diameter vasopressin (VP) neurons in the bed nucleus of the stria terminalis (BST) and medial amygdala (Me) which have been shown to exhibit steroid dependency and sexual dimorphism in many other rodent species. In rats, VP in the BST/Me is always colocalized with the neuropeptide galanin (GAL) and the sex difference in VP cell number appears to result from a sex difference in the number of GAL neurons which coexpress VP. Likewise, we reasoned that the species difference in extrahypothalamic VP pathways present in the golden hamster could result from a reduced coexpression of VP by GAL neurons in these regions. Here, we used in situ hybridization histochemistry to determine whether GAL mRNA expressing neurons are present in the BST and Me of golden hamsters despite the absence of VP expression in these regions. In addition, we have used slice binding and receptor autoradiography to identify specific GAL binding sites in the lateral septum, a probable target region of BST/Me neurons, and in situ hybridization to confirm that some of these binding sites correspond to the GALR1 GAL receptor subtype. Our findings indicate that the absence of VP expression in the BST/Me of golden hamsters results from a failure of extrahypothalamic GAL neurons to express the VP phenotype. Because GAL is expressed in the extended amygdaloid complex and GAL receptors are present in the septum of golden hamsters, GAL may play a role in modulating functions previously attributed to BST/Me pathways.
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PMID:Absence of vasopressin expression by galanin neurons in the golden hamster: implications for species differences in extrahypothalamic vasopressin pathways. 1010 Dec 29


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