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)

Neurophysins are neuropeptides (MW +/- 10,000) synthetized together with active nonapeptides vasopressin (AVP) and oxytocin (OT). The original description of the radioimmunoassay for neurophysins in 1969 allowed us to demonstrate the concomitant, equimolecular, release of them together with AVP and OT, thus bringing strong arguments in favour of neurohypophyseal exocytosis. Beside the use of those RIAs as direct indexes of neurohypophyseal release in various physiological and pathological conditions, we have been interested these last two years, to the putative use of neurophysins RIA as direct neuroendocrine markers in various neuropsychiatric diseases (depression, mania, schizophrenia) and paraneoplastic syndromes (SIADH).
Bull Mem Acad R Med Belg 1990
PMID:[Neurophysins]. 209 28

Retrograde amnesia was induced in rats trained in step-down inhibitory avoidance by four different treatments: an ip injection of beta-endorphin (1.0 microgram kg), an electroconvulsive shock (ECS), an intrahippocampal infusion of the calcium/calmodulin protein kinase II inhibitor, KN62 (0.08 microgram/side), given 0 h after training, or an intrahippocampal infusion of the protein kinase A inhibitor, KT5720 (0.5 microgram/side), given 3 h after training. Pretest ip injections of ACTH (0.2 microgram/kg) or vasopressin (10.0 micrograms/kg), but not saline, reversed the amnesia caused by beta-endorphin and ECS but not that caused by the enzyme inhibitors. This suggests that the amnesia produced by intrahippocampal KN62 and KT5720 administration is stronger than that caused by ECS and beta-endorphin, possibly because the former interfere directly with specific steps of the core biochemical chain of events that underlies memory consolidation.
Neurobiol Learn Mem 1997 Sep
PMID:Systemic administration of ACTH or vasopressin reverses the amnestic effect of posttraining beta-endorphin or electroconvulsive shock but not that of intrahippocampal infusion of protein kinase inhibitors. 932 61

We have sought to elucidate the biochemical mechanisms that underlie the memory enhancing properties of the neural peptide vasopressin. Toward that goal we have investigated vasopressin induction of calcium signaling cascades, long held to be involved in long-term memory function, in neurons derived from the cerebral cortex, a brain region associated with long-term memory. Our previous studies demonstrated that in cultured cortical neurons, V1a vasopressin receptor (V1aR) activation resulted in a sustained rise in intracellular calcium concentration that was dependent on calcium influx (Son & Brinton, 1998). To investigate the mechanism of V1aR-induced calcium influx, we investigated V1aR activation of the calcium channel subtype(s) in cortical neurons cultured from Sprague-Dawley rat embryonic day 18 fetuses. The results of these analyses demonstrated that the L-type calcium channel blocker nifedipine blocked 250 nM V1 vasopressin receptor agonist (V1 agonist)-induced calcium influx. Intracellular calcium imaging analyses using fura-2AM demonstrated that blockade of L-type calcium channels prevented the 250 nM V1 agonist-induced rise in intracellular calcium concentration. These results indicate that the influx of extracellular calcium via L-type calcium channels is an essential step in the initiation of the V1 agonist-induced rise in intracellular calcium concentration. To determine the mechanism of V1aR activation of L-type calcium channels, regulatory components of the phosphatidylinositol signaling pathway were investigated. The results of these analyses demonstrated that V1 agonist-induced calcium influx was blocked by both a phospholipase C inhibitor (U-73122) and a protein kinase C inhibitor (bisindolylmaleimide I). Further analysis of V1aR activation of protein kinase C (PKC) demonstrated that V1 agonist induced PKC activity within 1 min of exposure in cultured cortical neurons. These data indicate that in cultured cortical neurons, V1aR activation regulates the influx of extracellular calcium via L-type calcium channel activation through a protein kinase-C-dependent mechanism. The results of these studies provide biochemical mechanisms by which vasopressin could enhance memory function. Those mechanisms include a complex cascade that is initiated by activation of the phosphatidylinositol pathway, activation of protein kinase C, followed by phosphorylation of L-type calcium channels to initiate the influx of extracellular calcium to activate a cascade of calcium-dependent release of intracellular calcium.
Neurobiol Learn Mem 2001 Nov
PMID:Regulation and mechanism of L-type calcium channel activation via V1a vasopressin receptor activation in cultured cortical neurons. 1172 44

Oxytocin as an endogenous antistress hormone. The neurohypophysial peptide oxytocin (OT), besides it well known uterotonic and milk ejection activity, share also an inhibitory action on corticotrope activity. This has been demonstrated not only in pharmacological (perfusion) but also in physiological (lactation) conditions. This action is opposite to that of its "sister" hormone vasopressin (AVP) thus bringing arguments favouring the ago-antagonist ying-yang hypothesis. A non pharmacological stimulation of ocytocine secretion, as we have recently demonstrated in a preliminary study, related to hypnosis, could induce a beneficial inhibition of corticotrop axis and needs further rigorous experimental approach.
Bull Mem Acad R Med Belg 2002
PMID:[Oxytocin: a natural means of treating psychological stress]. 1264 77

The vasopressin (VP)/oxytocin (OT)-related peptides constitute a large superfamily found in a wide range of both vertebrate and invertebrate species. While intensive literature reports that these neuropeptides influence behavior, especially learning and memory, in numerous species from diverse vertebrate groups, their roles in behavioral regulation have never been studied in invertebrates. Here, we investigated the role of two VP/OT superfamily peptides, octopressin (OP) and cephalotocin (CT), on long-term memory (LTM) formation of a passive avoidance task in a cephalopod mollusc, the cuttlefish, Sepia officinalis. Subadult cuttlefish were intravenously injected, in a dose range of 3-60 microg/kg, 1h after the training phase (consolidation design); retention performance was tested 24h post-training. We found that administration of OP at low dose (3 microg/kg) enhanced LTM, whereas a dose of 60 microg/kg attenuated it. No effect of OP on LTM was observed for the 15 microg/kg dose. Conversely, an enhancement of retention performance was observed at all doses of CT tested. This study is the first to demonstrate the behavioral effects of VP/OT superfamily peptides in an invertebrate species. The valuable role of VP/OT-like peptides on memory processes offers new evolutionary perspectives on peptidergic transmission and neuromodulation.
Neurobiol Learn Mem 2010 Feb
PMID:Vasopressin/oxytocin-related peptides influence long-term memory of a passive avoidance task in the cuttlefish, Sepia officinalis. 1985 82

The abilities to recognize individual animals of the same species and to distinguish them from other individuals are the basis for all mammalian social organizations and relationships. These abilities, termed social recognition memory, can be explored in mice and rats using their innate tendency to investigate novel social stimuli more persistently than familiar ones. Using this methodology it was found that social recognition memory is mediated by a specific neural network in the brain, the activity of which is modulated by several molecules, such the neuropeptides oxytocin and vasopressin. During the last 15 years several independent studies have revealed that social recognition memory of mice and rats depends upon their housing conditions. Specifically, long-term social recognition memory cannot be formed as shortly as few days following social isolation of the animal. This rapid and reversible impairment caused by acute social isolation seems to be specific to social memory and has not been observed in other types of memory. Here we review these studies and suggest that this unique system may serve for exploring of the mechanisms underlying the well-known negative effects of partial or perceived social isolation on human mental health.
Neurobiol Learn Mem 2015 Oct
PMID:The effects of acute social isolation on long-term social recognition memory. 2616 36