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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of vasopressin on neurons of the rat dorso-lateral septum (DLS) was studied in brain slices with intracellular microelectrodes. Two out of 13 neurons showed a small depolarization, spontaneous activity, and increased input resistances following a 15 min exposure to 10(-6) to 10(-8) M vasopressin (VP). These membrane effects disappeared completely within 3-5 min after the application. The remaining DLS neurons treated with these vasopressin concentrations showed an increase in glutamate-mediated excitatory postsynaptic potentials (EPSPs), evoked by stimulation of the fimbria fibers. As little as 10(-12) MVP increased these EPSPs markedly in nearly 80% of the cells studied. This increase in most of the cells disappeared within 15 min after the application period, whereas the increase in EPSPs induced by 10(-10) M VP outlasted the peptide application period for more than 30 min. Neither the blockade of GABA-ergic synaptic inhibition nor the pre-treatment of the neurons with d(CH2)5-Tyr(Me)-arginine vasopressin or 2-amino-5-phosphonovaleric acid (2-APV), antagonists for the V1 type of vasopressin receptor and NMDA receptors, respectively, interfered with the EPSPs potentiating effect of the peptide. It is concluded that a type of vasopressin receptor other then the V1 type is involved in the long-lasting potentiation of the primarily non-NMDA receptor mediated transmission in DLS neurons.
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PMID:Vasopressin facilitates excitatory transmission in slices of the rat dorso-lateral septum. 197 60

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

Vasopressin and oxytocin neuroendocrine cells within the supraoptic nucleus display distinctive electrophysiological properties and differential responses to selected NMDA receptor (NR) antagonists. To determine if these differences might be due to NMDA receptor composition, we compared the expression of NR1, NR2A, NR2B, NR2C and NR2D subunit mRNAs in immunocytochemically identified vasopressin and oxytocin neuroendocrine cells. In contrast to NR1 subunit mRNA which was equally expressed in both vasopressin and oxytocin cells, NR2B and NR2C displayed very different expression patterns. In oxytocin cells, the NR2B subunit comprised the majority (65%) of the total NR2 expression with NR2C and NR2D contributing 6% and 27%, respectively. Vasopressin cells exhibited 5-fold higher NR2C (32%), approximately half as much NR2B mRNA (39%) and equivalent NR2D (31%). In vitro expression studies have shown that the NR1-NR2C subunit combination exhibits weaker magnesium block and higher affinity for glycine than NR1-NR2B. Thus, the high expression of NR2C in vasopressin cells relative to oxytocin cells may make these cells more susceptible to glutamatergic activation. These observations in vasopressin and oxytocin cells provide the basis for a working model to investigate how differential NMDA receptor composition may shape the neurophysiological properties of neurons.
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PMID:Differential expression of five N-methyl-D-aspartate receptor subunit mRNAs in vasopressin and oxytocin neuroendocrine cells. 907 68

Arginine-vasopressin (AVP) is a neuropeptide which facilitates learning and memory processes. We examinated the participation of NMDA receptors in beneficial effects of peptide. The results of our study show that noncompetitive antagonist of NMDA receptor-MK-801 impairs the effect of AVP on the consolidation of conditioned avoidance responses and antagonist of polyamines site-arcaine reduced advantageous effect of AVP on the retrieval of memory in passive avoidance situation.
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PMID:The estimation of interactions between arginine-vasopressin (AVP) and NMDA receptors in memory and learning processes. 932 37

Experiments were undertaken to compare effects of the NMDA and non-NMDA receptor antagonists, AP5 (40 microM) and NBQX (10 microM), on glutamate-induced firing in supraoptic oxytocin (OT) and vasopressin (VP) neurones in vitro. In putative OT neurones NBQX caused a significantly greater reduction in firing than AP5, whilst in putative VP neurones both antagonists reduced activity powerfully and to a similar extent. The relatively small effect of AP5 in putative OT neurones was unaffected by the removal of extracellular magnesium. These results suggest that glutamate-induced firing in putative OT neurones is predominantly controlled by non-NMDA receptors.
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PMID:Glutamate excitation of oxytocin neurones in vitro involves predominantly non-NMDA receptors. 936 30

This study determines the interaction between glutamate receptors and dehydration-induced drinking, vasopressin (AVP) release, plasma osmolality and c-fos expression in the brain of conscious rats. The NMDA receptor antagonist dizocilpine (100 nmol infused into the cerebral ventricles) suppressed drinking following either 22 h water deprivation or intragastric injection of hypertonic saline (1.5 M), attenuated the increased plasma vasopressin induced by dehydration, but had no effects on peripheral hyperosmolality caused by either water deprivation or injections of hypertonic saline. Dizocilpine had no inhibitory effects on feeding after 24 h food deprivation. Dizocilpine also suppressed c-fos expression induced by dehydration in the median preoptic nucleus (MPN), the supraoptic and paraventricular nuclei (SON and PVN), but did not influence c-fos expression in the subfornical organ (SFO). The non-NMDA receptor antagonists CNQX (400 nmol) or DNQX (60 nmol) affected neither the animals' drinking nor c-fos expression induced by dehydration. Double staining showed that suppression of c-fos expression following dizocilpine occurred in the NMDA R1 receptor containing neurons in the hypothalamus. These results suggest that the NMDA-type glutamate receptors may be involved in dehydration induced dipsogenic and neuroendocrinological responses. They complement our earlier findings that dizocilpine also attenuates drinking and c-fos expression following intraventricular infusions of angiotensin II.
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PMID:Effects of intracerebroventricular dizocilpine (MK801) on dehydration-induced dipsogenic responses, plasma vasopressin and c-fos expression in the rat forebrain. 951 65

Behavioral experiments have shown that the N-methyl D-aspartate (NMDA) subclass of glutamate receptor plays an important role in acquisition of emotional memory. Exposure of a rat to conditioned fear stimuli suppresses vasopressin (VP) release and augments oxytocin (OT) or prolactin (PRL) release from the pituitary. Present experiments aimed at investigating the effect of intraperitonially administered MK-801, an antagonist of NMDA receptor on the emotional memory associated with the suppressive VP and the augmentative OT or PRL responses to conditioned fear stimuli in male rats. MK-801 injected 30 min before training impaired the VP, OT and PRL responses to the testing fear stimuli. The antagonist injected after training, however, did not block the responses. MK-801 administered before testing impaired the previously acquired VP, OT and PRL responses to conditioned fear stimuli. In the experiments with non-associatively applied fear stimuli, MK-801 did not block the VP, OT or PRL response. In the experiments with novel environmental stimuli, MK-801 did not impair VP, OT or PRL responses. The results suggest that an activation of NMDA receptors are required to acquire and recall but not to consolidate or retain the emotional memory associated with VP, OT and PRL responses to conditioned fear stimuli.
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PMID:Role of NMDA receptors in the emotional memory associated with neuroendocrine responses to conditioned fear stimuli in the rat. 959 38

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

Previous experiments demonstrated that excitatory amino acids participate in the osmotic regulation of vasopressin secretion, but the specific involvement of N-methyl-D-aspartic acid (NMDA) receptors was not evaluated. This was demonstrated in the present studies. NMDA stimulated vasopressin release from perifused explants of the hypothalamo-neurohypophyseal system (HNS), and osmotic stimulation of vasopressin release was inhibited by MK-801 (10 microM) and AP5 (100 microM) NMDA receptor antagonists. The effective concentration of NMDA was dependent upon the Mg2+ concentration of the perifusate with stimulation observed at 1 microM NMDA in Mg2+-replete compared with 5 microM in low-Mg2+ medium. Previous experiments also demonstrated that estradiol and dihydrotestosterone (DHT) inhibited osmotically stimulated vasopressin secretion, and a nongenomic mechanism of action was suggested by the ability of steroids conjugated to bovine serum albumin to replicate the effect. Experiments were performed to explore the potential role of NMDA receptors in this mechanism. Estradiol (50 pg/ml) and DHT (3 ng/ml) inhibited NMDA stimulated vasopressin release in perifused HNS explants. These results suggest a role of NMDA receptors in the mediation of vasopressin secretion in osmotically stimulated release. Furthermore, estradiol and DHT may exert their inhibitory effect on osmotically stimulated vasopressin release via the NMDA receptor.
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PMID:N-methyl-D-aspartic acid stimulation of vasopressin release: role in osmotic regulation and modulation by gonadal steroids. 974 85

The effects of arginine-vasopressin (AVP) on area postrema (AP) neurons and the neuronal connection between the AP and nucleus tractus solitarii (NTS) were electrophysiologically investigated in rat medulla slices. In the AP, 27.9% of 129 neurons were excited by AVP and 20.5% were inhibited. The excitation was blocked by an V1 receptor antagonist. Synaptic transmission of the AP to the NTS was mainly mediated by non-N-methyl-D-aspartate (NMDA) receptors. Local application of AVP to the AP activated the NTS neurons. This excitation was also blocked by an NMDA antagonist. These results suggest that the excitation originating in the AP is conveyed to the NTS via non-NMDA receptors and then modified by NMDA receptor activation secondly. These processes may be important in the regulation of the arterial baroreceptor reflex.
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PMID:Effects of arginine-vasopressin on neuronal interaction from the area postrema to the nucleus tractus solitarii in rat brain slices. 983 13


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