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)

1. Vasopressin-secreting neurones in the rat hypothalamic supraoptic nucleus display patterned spontaneous phasic activity, which is apparently maintained in vivo through yet unidentified neurotransmitter system(s). The present investigation used extracellular recording techniques in anaesthetized Long-Evans rats to evaluate whether the neurotransmitter mechanism underlying phasic firing is provided via a family of ionotropic glutamate receptors. 2. N-Methyl-D-aspartate (NMDA) reliably evoked bursts of activity in twenty-seven of twenty-eight phasic neurones. Amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) and kainate also elicited pronounced excitations in twenty-one of twenty-one and and fourteen of fifteen phasic cells, respectively. 3. A rapid blockade of on-going phasic activity was consistently induced following brief applications of both NMDA and non-NMDA receptor antagonists; extended application of antagonists resulted in prolonged silent periods, during which phasic activity failed to recur for minutes. Neither saline nor a cholecystokinin receptor antagonist influenced cell firing. 4. In contrast to putative vasopressin cells, application of NMDA receptor ligands did not affect the spontaneous activity in most putative oxytocin-secreting neurones, whereas kainate and AMPA potently excited seven of nine and four of five putative oxytocin cells, respectively. 5. These results imply that the maintenance of spontaneous phasic discharges in vivo in supraoptic vasopressin-secreting neurones requires tonic synaptic activation involving both NMDA and non-NMDA glutamate receptors. In putative oxytocin-secreting neurones, spontaneous firing appears to be predominantly regulated by non-NMDA receptors. Glutamatergic innervations may be in a unique position to influence the genesis of patterned electrical activity in supraoptic vasopressin neurones.
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PMID:Regulation of spontaneous phasic firing of rat supraoptic vasopressin neurones in vivo by glutamate receptors. 754 68

The amiloride-sensitive epithelial Na+ channel is formed by the assembly of three homologous subunits, alpha, beta and gamma. The channel is characterized by its sensitivity to amiloride and to some amiloride derivatives, such as phenamil and benzamil, by its small unitary conductance (approximately 5 pS), by its high selectivity for lithium and sodium, and by its slow kinetics. The alpha-, beta-, and gamma-proteins share significant identity with degenerins, a family of proteins found in the mechanosensory neurons and interneurons of the nematode Caenorhabditis elegans. They are also homologous to FaNaCh, a protein from Helix aspersa nervous tissues, which corresponds to a neuronal ionotropic receptor for the Phe-Met-Arg-Phe-NH2 peptide. All these proteins contain a large extracellular loop, located between two transmembrane alpha-helices. The NH2 and COOH terminal segments are cytoplasmic and contain potential regulatory segments that are able to modulate the activity of the channel. Accordingly, in Liddle syndrome, in which patients develop a form of genetic hypertension, mutations within the cytoplasmic COOH terminal of the beta- and gamma-chains of the epithelial Na+ channel lead to a hyperactivity of the channel. Epithelial Na+ channel activity is tightly controlled by several distinct hormonal systems, including corticosteroids and vasopressin. In kidney and colon, aldosterone is the major sodium-retaining hormone, acting by stimulation of Na+ reabsorption through the epithelium. In the distal colon from steroid-treated animals, a large increase in beta- and gamma-subunit transcription is observed, whereas the alpha-subunit remains constitutively transcribed. In kidney, RNA levels of the three subunits are not altered by aldosterone, suggesting that other mechanisms control Na+ channel activity in that tissue. In lung, the glucocorticoids are positive regulators of the channel activity, especially around birth, and act via an increased transcription of the three subunits.
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PMID:Molecular biology of the amiloride-sensitive epithelial Na+ channel. 873 81

Atrial natriuretic peptide (ANP) and its receptors are present in hypothalamic nuclei containing the magnocellular neurosecretory cells (MNCs), which release vasopressin and oxytocin. In the rat, intracerebroventricular injections of ANP inhibit the release of both hormones in response to hypertonicity. Although these findings suggest a role for endogenous ANP in the central control of fluid balance, cellular mechanisms underlying the modulatory actions of ANP are unknown. We therefore examined the effects of ANP on the osmoresponsiveness of MNCs impaled in rat hypothalamic explants. Applications of ANP (75-150 nM) over the supraoptic nucleus did not affect depolarizing responses to local hypertonicity, but they reversibly abolished the synaptic excitation of MNCs after hypertonic stimulation of the organum vasculosum laminae terminalis (OVLT). These effects were associated with decreased spontaneous EPSP (sEPSP) amplitude rather than with changes in sEPSP frequency. Accordingly, application of ANP reduced the amplitude of glutamatergic EPSPs evoked by electrical stimulation of the OVLT (IC50 approximately 3 nM). The inhibitory effects of ANP on EPSP amplitude were mimicked by application of 3'-5'-dibutyryl cGMP, consistent with the guanylate cyclase activity of natriuretic peptide receptors. Although depolarizing responses of MNCs to ionotropic glutamate receptor agonists were unaffected by ANP, the peptide reversibly enhanced paired-pulse facilitation of electrically evoked EPSPs. These results indicate that centrally released ANP may inhibit osmotically evoked neurohypophysial hormone release through presynaptic inhibition of glutamate release from osmoreceptor afferents derived from the OVLT.
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PMID:Atrial natriuretic peptide modulates synaptic transmission from osmoreceptor afferents to the supraoptic nucleus. 892 8

The amiloride-sensitive epithelial Na+ channel is formed by the assembly of three homologous subunits alpha, beta and gamma. The channel is characterized by its sensitivity to amiloride and to some amiloride derivatives, such as phenamil and benzamil, by its small unitary conductance (approximately 5pS), by its high selectivity for lithium and sodium, and by its slow kinetics. The alpha, beta, and gamma proteins share significant identity with degenerins, a family of proteins found in the mechanosensory neurons and interneurons of the nematode Caenorhabditis elegans. They are also homologous to FaNaCh, a protein from Helix aspersa nervous tissues, which corresponds to a neuronal ionotropic receptor for the Phe-Met-Arg-Phe-amide peptide. All these proteins contain a large extracellular loop, located between two transmembrane alpha-helices. The NH2 and COOH terminal segments are cytoplasmic, and contain potential regulatory segments that are able to modulate the activity of the channel. In Liddle syndrome, in which patients develop a form of genetic hypertension, mutations within the cytoplasmic COOH terminal of the beta and gamma chains of the epithelial Na+ channel lead to a hyper-activity of the channel. Epithelial Na+ channel activity is tightly controlled by several distinct hormonal systems, including corticosteroids and vasopressin. In kidney and colon, aldosterone is the major sodium-retaining hormone, acting, by stimulation of Na+ reabsorption through the epithelium. In the distal colon from steroid-treated animals, a large increase of the beta and gamma subunits transcription is observed, whereas the alpha subunit remains constitutively transcribed. In kidney, RNA levels of the three subunits are not significantly altered by aldosterone, suggesting that other mechanisms control Na+ channel activity in that tissue. In lung, the glucocorticoids are the positive regulators of the channel activity, especially around birth, and act via an increased transcription of the three subunits.
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PMID:[The amiloride sensitive sodium channel]. 901 66

For better understanding of glial participation in cerebral ischemia, spectrofluorimetric analysis using the calcium indicator Fura-2AM was applied to examine the role of intracellular free Ca2+ ([Ca2+])i elevation induced by different neuroactive substances in cultured rat brain astrocytes. The activation by the general receptor agonist glutamate resulted in a biphasic cell response in [Ca2+]i. We couldn't observe N-methyl-D-aspartate-evoked [Ca2+]i response at all. Quisqualate triggered a complex [Ca2+]i response in astrocytes consisting of mobilization of Ca2+ from the intracellular stores and also Ca2+ influx from the extracellular space. Kainate elicited a markedly different Ca2+ signal an external Ca(2+)-dependent sustained [Ca2+]i rise resulting from the activation of the ionotropic glutamate receptor. According to our results two types of glutamate receptors, the quisqualate-specific metabotropic and kainate-specific ionotropic receptor, are involved in [Ca2+]i elevation in these cultures. We could monitor agonist-specific cell response to noradrenaline, serotonin, vasopressin and ATP as well in these cultured rat astrocytes.
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PMID:Intracellular free Ca2+ elevations in cultured astroglia induced by neuroligands playing a role in cerebral ischemia. 940 2

The mechanism of facilitatory action of vasopressin on memory processes, dependent probably on different neurotransmitter systems, remains unclear. We decided to study the interactions between arginine-vasopressin and ionotropic NMDA receptor. We estimated the influence of various antagonists of NMDA receptor on beneficial effect of arginine-vasopressin on consolidation of conditioned avoidance responses and on retrieval of memory in passive avoidance situation. We have shown that effect of vasopressin on consolidation is significantly reduced by noncompetitive antagonist of ion channel in the NMDA receptor--dizocilpine (MK-801) and competitive antagonist of glycine recognization site--HA-966. Distinctly, effect of the peptide on retrieval is decreased by competitive antagonist of glutamate recognition site--AP-7, competitive antagonist of polyamines site-arcaine and noncompetitive antagonist--MK-801. This suggests that NMDA receptor may participate in the action of vasopressin on memory, but it plays different roles in consolidation and retrieval processes.
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PMID:Role of NMDA receptor in the effects of arginine-vasopressin on memory processes. 966 33

The neurosteroid pregnenolone sulphate (PS) interacts allosterically with ionotropic glutamate receptors and thereby could be an important modulator of activity within the hypothalamic magnocellular nuclei. The present in-vitro study therefore examined the effect of perifusion of PS (100 microM) on activity of supraoptic oxytocin (OT) and vasopressin (VP) neurones, in which firing was stimulated by local application of glutamate, NMDA or AMPA. In the presence of locally applied glutamate, PS significantly potentiated firing in putative VP neurones, but had little effect on putative OT neurones. In both cell types, PS increased firing in the presence of NMDA and depressed firing in the presence of AMPA. The action of PS on glutamate- and NMDA-stimulated firing was unaffected by addition of the GABA(A) receptor antagonist, picrotoxin (50 microM). The suppressive action of PS on AMPA-stimulated firing was, however, reversed by picrotoxin and therefore probably requires intact GABAergic transmission for its expression. When putative VP neurones were stimulated by local application of K+, in the presence of picrotoxin, PS evoked a small increase in the ongoing activity, although this did not reach significance. When the glutamate receptor antagonists, NBQX (20 microM) and AP5 (40 microM), were included in the medium, no change in K+ -stimulated firing was observed. Hence PS has no effect on activity of putative VP neurones in the absence of exogenous and endogenous glutamate excitation. In conclusion, PS selectively potentiates glutamate-stimulated activity in putative VP neurones, probably via NMDA receptors, thus providing a mechanism whereby this neurosteroid might exert rapid non-genomic effects on VP secretion. The lack of effect of PS in putative OT neurones probably relates to the relatively small involvement of NMDA receptors in mediating glutamate excitation in this cell type.
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PMID:Supraoptic oxytocin and vasopressin neurones show differential sensitivity to the neurosteroid pregnenolone sulphate. 983 Dec 59

Noradrenergic projections to the hypothalamus play a critical role in the afferent control of oxytocin and vasopressin release. Recent evidence for intrahypothalamic glutamatergic circuits prompted us to test the hypothesis that the excitatory effect of noradrenergic inputs on oxytocin and vasopressin release is mediated in part by local glutamatergic interneurons. The voltage response to norepinephrine (30-300 microM) was tested with whole-cell recordings in putative magnocellular neurons of the paraventricular nucleus (PVN) in hypothalamic slices (400 micrometers). Norepinephrine elicited an alpha1 receptor-mediated direct depolarization in 23% of the magnocellular neurons tested; however, the most prominent response, seen in 42% of the magnocellular neurons, was an alpha1 receptor-mediated increase in the frequency of EPSPs. The norepinephrine-induced increase in EPSPs was blocked by tetrodotoxin and by ionotropic glutamate receptor antagonists, suggesting that norepinephrine excited presynaptic glutamate neurons to cause an increase in spike-mediated transmitter release. The increase in EPSPs also was observed in a surgically isolated PVN preparation (64% of cells) and with microdrop applications of norepinephrine (1 mM, 33% of cells) and glutamate (0.5-1 mM, 28%) in the PVN, indicating that the norepinephrine-sensitive presynaptic glutamate neurons are located within the PVN. Biocytin injection and subsequent immunohistochemical labeling revealed that both oxytocin and vasopressin neurons responded to norepinephrine. Our data indicate that magnocellular neurons of the PVN receive excitatory inputs from intranuclear glutamatergic neurons that express alpha1-adrenoreceptors. These glutamatergic interneurons may serve as an excitatory relay in the afferent noradrenergic control of oxytocin and vasopressin release under certain physiological conditions.
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PMID:Noradrenergic excitation of magnocellular neurons in the rat hypothalamic paraventricular nucleus via intranuclear glutamatergic circuits. 985 97

The excitatory amino acid glutamate, acting via ionotropic and metabotropic glutamate receptors, appears to play an important role in the control of neuroendocrine functions. The aim of the present investigations was to determine whether hypothalamic neurones which synthesize arginin-vasopressin (AVP), CRF and VIP express metabotropic glutamate receptor (mGluR). Double-label immunocytochemistry and the mirror technique were used. We found that AVP immunoreactive neurones of the paraventricular, supraoptic and suprachiasmatic nuclei contain mGluR1a, but the number of double-labelled neurones was different in the three cell groups. mGluR1a was present in a significant number of paraventricular CRF nerve cells, and in almost all VIP neurones of the SCHN. These results support the view that the excitatory transmitter glutamate may directly influence AVP, CRF and VIP neurones of the three hypothalamic cell groups.
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PMID:Metabotropic glutamate receptor in vasopressin, CRF and VIP hypothalamic neurones. 992 42

Gene expression studies advance our understanding of the effects of stress and glucocorticoids on brain function and give a new direction to animal welfare research. In this context, the presence of messenger RNA s (m RNA s) for corticotrophin releasing hormone (CRH) and vasopressin (VP) in the porcine hypothalamus has recently been documented. This study investigated the expression of CRH, VP and ionotropic glutamate receptor (iGluR) subunit m RNA s in the brains of pigs treated with the synthetic glucocorticoid dexamethasone (Dex; 5 mg kg(-1)i.v.). In the hypothalamus, VP, but not CRH, m RNA was reduced 3 hours after Dex. In the hippocampus, expression of m RNA s for some iGluR subunits appeared to be differentially regulated 6 hours after Dex. In addition, CRH message was detected in the hippocampus and significantly upregulated in the CA1 region 3 hours after Dex. The relevance of these findings to stress neurobiology of the growing pig is discussed.
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PMID:Gene expression in the forebrain of dexamethasone-treated pigs: effects on stress neuropeptides in the hypothalamus and hippocampus and glutamate receptor subunits in the hippocampus. 1092 90


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