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Query: UNIPROT:P01178 (oxytocin)
 15,767 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

The neuropeptides arginine vasopressin (AVP) and oxytocin (OT) have been thought to play a significant role in behavioral regulation in general and in learning and memory in particular. Experimental evidence suggests that AVP improves, and OT impairs, learning and memory. The present paper investigates the posttraining effects of OT and of an OT receptor antagonist, and their interaction, on memory storage in mice. Additional studies were conducted to determine the specificity of the interaction between OT and its receptors. Male Swiss mice were tested 48 h after training in a one-trial step-through inhibitory avoidance task. Immediate posttraining subcutaneous injection of OT (0.01, 0.03, 0.10, 0.30, and 1.00 microg/kg) impaired retention performance. The dose-response curve showed a U-shaped form, with a significant impairment seen at doses of 0.10 and 0.30 microg/kg of OT. In contrast, the immediate posttraining administration of the putative oxytocin receptor antagonist d(CH2)5[Tyr(Me)2, Thr4, Thy-NH(9)2]OVT (AOT, 0.03, 0.10, 0.30, and 1.00 microg/kg) significantly enhanced retention performance. The dose-response curve was an inverted "U" in this range of doses. However, of the doses tested, only 0.30 microg/kg was effective. Neither OT nor AOT affected response latencies in mice not given the footshock on the training trial, indicating that the actions of both treatments on retention performance were not due to nonspecific proactive effects on response latencies. Neither the imparing effects of OT (0.10 microg/kg) nor the enhancing effects of AOT (0.30 microg/kg) were seen when the training-treatment interval was 180 min, suggesting that both treatments influenced the storage of recently acquired information. The effects of OT (0.10 microg/kg) on retention were prevented by AOT (0.03 microg/kg) administered immediately after training, but 10 min prior to oxytocin treatment. This dose of antagonist did not affect retention by itself, either under the standard experimental conditions or in mice trained with a lower level of footshock. On the contrary, OT (0.10 microg/kg) impaired retention in mice pretreated with the V1a vasopressin receptor antagonist d(CH2)5[Tyr(Me)2]AVP (0.01 microg/kg), which, however, was able to prevent the enhancement of retention induced by posttraining administration of AVP (0.03 microg/kg). Finally, the effects of AVP (0.03 microg/kg) on retention were not prevented by AOT (0.03 microg/kg). Considered together, these findings suggest that the impairment of retention of an inhibitory avoidance response in mice induced by posttraining oxytocin is probably due to an interaction of the neuropeptide with specific receptors.
Neurobiol Learn Mem 1998 Mar
PMID:Effects of a single administration of oxytocin or vasopressin and their interactions with two selective receptor antagonists on memory storage in mice. 961 93

Oxytocin (OT, 0.10 microg/kg, sc) impaired retention of a one-trial step-through inhibitory avoidance task when injected into male Swiss mice 10 min after training, as indicated by retention performance 48 h later. In contrast, the immediate post-training administration of the putative oxytocin receptor antagonist d(CH(2))(5)[Tyr(Me)(2), Thr(4), Thy-NH(9)(2)] OVT (AOT, 0.30 microg/kg, sc) significantly enhanced retention performance. Neither OT nor AOT affected response latencies in mice not given footshock on the training trial, and neither the impairing effects of OT nor the enhancing effects of AOT were seen when the training-treatment interval was 180 min, suggesting that both treatments influenced memory storage. The effects of OT (0.10 microg/kg, sc) on retention were prevented by AOT (0.03 microg/kg, sc) given immediately after training, but 10 min prior to OT treatment. The central acting anticholinesterase physostigmine (35, 70, or 150 microg/kg, i.p.), but not its quaternary analogue neostigmine (150 microg/kg, i.p.), reversed the impairment of retention performance induced by OT, whereas low subeffective doses of the centrally active muscarinic cholinergic antagonist atropine (0.5 mg/kg, i.p.) or the central acting nicotinic cholinergic antagonist mecamylamine (5 mg/kg, i.p.), but not methylatropine (0.5 mg/kg, i.p.) or hexamethonium (5 mg/kg, i.p.) prevented the enhancement of retention performance caused by AOT. We suggest that oxytocin negatively modulates the activity of central cholinergic mechanisms during the posttraining period that follows an aversively motivated learning experience, leading to an impairment of retention performance of the inhibitory avoidance response.
Neurobiol Learn Mem 2000 Nov
PMID:Involvement of central cholinergic mechanisms in the effects of oxytocin and an oxytocin receptor antagonist on retention performance in mice. 1103 Nov 28

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

During the last decade, a considerable amount of evidence has accumulated to show that oxytocin (OT) is involved with functions other than its classical roles in reproduction-associated processes, such as social recognition, maternal behavior and neuroendocrine regulation of the stress response. It has been shown, for instance, that post-training systemic administration of oxytocin in mice produces an amnestic effect on the step-through inhibitory avoidance. Since it is still unclear how systemic levels of OT may affect CNS memory processes, our aim here was to investigate the hypothesis that systemic OT effects on memory retrieval might be mediated through an oxytocin-induced decrease in glucocorticoid release. In our first experiment, we have found an amnestic effect of i.p. pre-test 0.4 microg/kg of OT upon memory retrieval in the inhibitory avoidance task (IA); this OT dose was shown to (a) significantly decrease plasma corticosterone levels when compared to the saline group, and (b) not to cause any anxiety effects by itself in a plus-maze task. At last, an ineffective-by-itself dose of dexamethasone was able to reverse the amnestic effect of this OT dose. Our results suggest that the amnestic effect of systemically administered oxytocin upon memory retrieval in the inhibitory avoidance task was probably caused by an oxytocin-induced decrease in glucocorticoid release from the adrenal gland.
Neurobiol Learn Mem 2007 Jan
PMID:Glucocorticoid-mediated effects of systemic oxytocin upon memory retrieval. 1699 85

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 present study investigated how oxytocin (OT) signaling in the central (CeA) and basolateral (BLA) amygdala affects acquisition, expression, and extinction of context-conditioned fear (freezing) in rats. In the first set of experiments, acquisition of fear to a shocked context was impaired by a preconditioning infusion of synthetic OT into the CeA (Experiment 1) or BLA (Experiment 2). In the second set of experiments, expression of context fear was enhanced by a pre- or post-extinction CeA infusion of synthetic OT (Experiments 3-6) or a selective OT receptor agonist, TGOT (Experiment 4). This enhancement of fear was blocked by coadministration of an OT receptor antagonist, OTA (Experiment 5) and context fear was suppressed by administration of the antagonist alone (Experiment 6). In the third set of experiments, expression of context fear was suppressed, not enhanced, by a preextinction BLA infusion of synthetic OT or a selective OT receptor agonist, TGOT (Experiments 7 and 8). This suppression of fear was blocked by coadministration of the OT receptor antagonist, OTA (Experiment 8). Taken together, these findings show that the involvement of the CeA and BLA in expression and extinction of context-conditioned fear is dissociable, and imply a critical role for oxytocin signaling in amygdala-based regulation of aversive learning.
Learn Mem 2015 May
PMID:Oxytocin signaling in basolateral and central amygdala nuclei differentially regulates the acquisition, expression, and extinction of context-conditioned fear in rats. 2587 37

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

Remembering and forgetting are fundamental features of an organism. Extinction is a type of forgetting where there is a decrease in the significance and/or the meaning of an associative memory when elements of that memory no longer predict one another. The neural mechanisms underlying extinction of fear memories have been extensively studied in the laboratory because extinction processes are clinically relevant to exposure therapies that treat anxiety disorders. However, only in the last decade have we begun to unveil the similarities and differences in plasticity underlying extinction across development. So far it is clear that extinction is a developmentally dissociated process in behavior and in pharmacology, however there are many large gaps in the literature in understanding how the developmental trajectory of different neurotransmitters contribute to changes in the nature of extinction across development. We attempt to address these gaps in the present review. Major neurotransmitter systems including the glutamatergic and GABAergic systems, the monoamines, the endogenous opioid and cannabinoid systems, acetylcholines, and neuropeptides such as oxytocin have all been identified to play some role in extinction of fear memories and have been covered in this review. We hope to facilitate more research into mechanisms of extinction at different stages of life, especially noting that mental disorders are increasingly classified as neurodevelopmental disorders.
Neurobiol Learn Mem 2017 Feb
PMID:Postnatal development of neurotransmitter systems and their relevance to extinction of conditioned fear. 2781 67

A growing body of evidence suggests that the hypothalamic neuropeptide oxytocin (OT), aside from its central role in the regulation of social behavior, reduces fear and anxiety. The functional and opposing interactions of the medial prefrontal cortex (mPFC) and the amygdala in regulation of fear provide a unique experimental setting to examine the effects of OT on fear and extinction. Recent evidence suggests that in the adult animal OT can play a dual role in the regulation of fear leading to contrasting effects on fear depending on the manipulated brain region and the time of manipulations. The OT system is one of the systems that undergoes major changes throughout development, however, its role in regulating fear in young animals has not been widely explored. We recently showed that the mechanisms of extinction, and specifically engagement of the mPFC in extinction, are not identical in adult and juvenile animals. Thus, the purpose of this study was to elucidate the effects of OT on fear and extinction in juvenile animals. To that end, we determine extinction, by measuring freezing at different time points, following microinjection of the OT agonist, TGOT, into the mPFC, the basolateral and the central nuclei of the amygdala (BLA and CeA, respectively). The results show that whereas TGOT microinjections into the IL-mPFC did not affect extinction, microinjections into the amygdala were mainly associated with enhanced fear and impaired extinction. These results further emphasize the differences between adult and juvenile brains.
Neurobiol Learn Mem 2017 May
PMID:Oxytocin in the amygdala and not the prefrontal cortex enhances fear and impairs extinction in the juvenile rat. 2838 81


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