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)

Localization of oxytocin- and vasopressin-binding sites has so far been studied in the rat brain by means of film autoradiographs. The disposal of iodinated ligands with high specificity has allowed us to develop histoautoradiography on emulsion-coated sections and to reinvestigate on a microscopic scale the distribution of these sites in the telencephalon (septum, striatopallidal system, amygdala and hippocampus). This technique showed that oxytocin and vasopressin labelling presented distinct distributions and coincided with delimited zones, corresponding to anatomical subdivisions defined on cytoarchitectural and immunocytochemical bases. Vasopressin sites were seen in the dorsal and intermediate parts of the lateral septum and the juxtacapsular nucleus of the bed nucleus of the stria terminalis. Oxytocin sites were located in the ventral and intermediate parts of the lateral septum, the oval and the principal nuclei of the bed nucleus of the stria terminalis and the septofimbrial nucleus. In the striatopallidal system, vasopressin sites were found in the accumbens nucleus and the fundus striati, whereas oxytocin sites were in the accumbens nucleus, the head, and the posterolateral parts of the caudate-putamen, the striatal cell bridges, and the olfactory tubercle. In the amygdala, vasopressin sites were not found, but oxytocin sites were located in the central, medial, and basomedial nuclei. In the hippocampus, vasopressin sites were located in the dentate gyrus (polymorph and molecular layers), and oxytocin sites, in the subiculum (molecular and pyramidal layers) and in the field CA1 of Ammon's horn (lacunosum moleculare and pyramidal layers). The localization of the binding sites at the microscopic level permitted us to reinvestigate whether or not correlation existed in a same area between innervation, electrophysiological effects, and presence of binding sites.
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PMID:Histoautoradiographic detection of oxytocin- and vasopressin-binding sites in the telencephalon of the rat. 839 91

In order to establish whether vasopressin (VP) influences brain cell survival, [3H]thymidine was injected in 10-day-old vasopressin-deficient Brattleboro rat pups, as well as in Wistar pups treated, neonatally, with the VP antagonist dP[Tyr(Me)2]VP followed by subsequent measurement of [3H]DNA in olfactory bulbs and cerebellum days and weeks thereafter. Results show, first of all, that the incorporation of [3H]thymidine into DNA was enhanced in the homozygous (HOM) Brattleboro, when compared with the heterozygous (HET; non-vasopressin-deficient) controls. The difference is due to the greater and prolonged tissue availability of [3H]thymidine, possibly pointing to an altered thymidine uptake and/or metabolism. Between postnatal days 25 and 39 no differences were seen in [3H]DNA content of the brain parts of the HET and Wistar control rats. For the HOM rats, however, a loss of [3H]DNA was seen (up to 8%), indicating that increased postnatal brain cell death might occur in the mutant. The antagonist treatment in Wistar rat up to 21 days of age failed to show a similar effect. It is proposed that general growth impairments, rather than VP receptor-mediated effects, lead to the brain cell loss.
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PMID:Increased loss of brain DNA in the neonatal vasopressin-deficient Brattleboro rat, but not in normal rat treated with vasopressin antagonist. 841 82

Social transmission of information was tested in a procedure in which a rat (Observer) could demonstrate preference for a flavored tea as drinking solution that a con-specific (Demonstrator) had consumed just prior to a period of social interaction between the two animals. The cue in this procedure, probably olfactory in nature, was remembered for a relatively short period of time. It was prolonged when the Observers were treated with dresglycinamide[Arg8]-vasopressin (DGAVP) or oxytocin immediately after the encounter with the Demonstrator. DGAVP was effective after the injection of 15 micrograms.kg-1 but not of 1.5 ng.kg-1. Oxytocin induced the effect in doses ranging from 1.5 ng.kg-1 to 15 micrograms.kg-1. A dose of 0.15 ng.kg-1 was inactive. The influence of the peptides was cue specific. It is concluded that DGAVP and oxytocin facilitate social transmission of information, as previously found for social recognition.
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PMID:Social transmission of flavored tea preferences: facilitation by a vasopressin analog and oxytocin. 844 34

In Mongolian gerbils, the content of vasopressin in the cerebral cortex, the striatum, and the hypothalamus is increased after induction of acute cerebral ischemia. We used an iodinated vasopressin analogue and light microscopic autoradiography to study the distribution of vasopressin V1 receptors in the brain of adult male gerbils and to evaluate the effects of a transient bilateral cerebral ischemia (6 minutes) on the density of this receptor population. The animals were killed immediately or 10, 30, or 100 hours after transient bilateral occlusion of the common carotid arteries. In control animals, specific [125I]-VPA binding sites were present in various structures of the brain (olfactory bulb, anterior olfactory nucleus, lateral septum, bed nucleus of the stria terminalis, median preoptic area, ventral pallidum, substantia innominata, amygdala, thalamus, hypothalamic mammillary nuclei, superior colliculus, subiculum, central gray, nucleus of the solitary tract, hypoglossal nucleus). The strongest labeling was detected in the cerebral cortex, layers 5-6. After 30-100 hours of survival time following ischemia there was a marked decrease in [125I]-VPA binding site density in these cerebral cortex layers. To a lesser degree, a decrease was also detected in the lateral septal nucleus. In contrast, labeling in other noncortical structures remained unchanged. All animals with 100 hours recovery showed a loss of cells in hippocampus (CA1 layer) and striatum. In addition, ischemia induced concomitant and proliferative changes in cortical and hippocampal astrocytes assessed by glial fibrillary acid protein immunoreactivity. These observations indicate a role for vasopressin in the cerebral cortex either on neurons or on glial cells and the modulation of vasopressin receptor expression by transient cerebral ischemia.
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PMID:Vasopressin binding in the cerebral cortex of the Mongolian gerbil is reduced by transient cerebral ischemia. 857 35

Activating direct olfactory (glutamatergic) inputs to supraoptic nucleus (SON) neurons increases interneuronal coupling in slices from lactating but from not virgin or male rats. Studied here were influences on coupling of another monosynaptic input to SON, the histaminergic tuberomammillary nucleus (TM) projection, activation of which selectively excites phasically firing (putative vasopressin) cells. Effects of TM stimulation and its possible downstream consequences on Lucifer yellow (LY) dye coupling among putative vasopressin cells were determined in male rat SONs. In unstimulated slices, 12 LY injections (1 cell/SON) yielded eight single and four pairs of coupled neurons. In slices in which TM was stimulated for 10 min at 10 Hz, 13 injections yielded 4 single and 28 coupled cells, with groups of 2 to 4 cells coupled to the injected neuron, a threefold increase in the number of coupled cells per injection (p < 0.02). Bathing slices in medium containing 10 microM pyrilamine (H1 antagonist) blocked this stimulation-induced coupling increase, suggesting mediation by activation of guanylate cyclase-cGMP to which H1 receptors often are linked . Bathing slices in medium containing 0.5-1 mM 8-bromo-cGMP yielded results similar to those of TM stimulation, a 2.5-fold increase over control in the number of coupled cells per injection. Effects of TM stimulation on coupling also were blocked by bathing slices in a guanylate cyclase inhibitor (10 microM LY83583). In contrast to cGMP, 1 mM 8-bromo-cAMP significantly reduced coupling. We conclude that synaptically released histamine increases coupling via cGMP-dependent mechanisms.
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PMID:Synaptically released histamine increases dye coupling among vasopressinergic neurons of the supraoptic nucleus: mediation by H1 receptors and cyclic nucleotides. 861 78

The effects of electrical stimulation of the hypothalamus paraventricular nucleus on the spontaneous firing of mitral and granule cells in the main olfactory bulb were examined in ovariectomized female rats under urethane anaesthesia. High-frequency stimulation (0.5-1.0 mA, 10-20 pulses at 100 Hz) of the paraventricular nucleus produced inhibitory responses in 80% of mitral cells tested and excitatory responses in 74% of granule cells tested, with latencies ranging from 2 to 150 s. Both responses were blocked by infusions into the olfactory bulb of [d(CH2)5, Tyr(Me)2]ornithine-vasotocin (10 pmol), an oxytocin antagonist, and mimicked by intracerebroventricular infusions (0.2 or 0.4 nmol) or microiontophoretic applications of oxytocin but not by intracerebroventricular infusions of vasopressin (1 or 2 nmol). Infusions of 0.5% lignocaine, a local anaesthetic, into either the medial olfactory tract or the medial forebrain bundle failed to block the responses of mitral and granule cells to the stimulation. Unilateral transections at various levels between the bulb and the paraventricular nucleus also failed to block the responses. There were cases in which significant responses of mitral and granule cells to the stimulation required 60 or more pulses after the lignocaine infusions or transections, however. These results suggest that oxytocin originating in the hypothalamic paraventricular nucleus reaches the olfactory bulb following its release partly into the cerebrospinal fluid and acts to decrease olfactory processing.
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PMID:The action of oxytocin originating in the hypothalamic paraventricular nucleus on mitral and granule cells in the rat main olfactory bulb. 873 30

The terminal nerve is a ganglionated cranial nerve with peripheral processes that enter the nasal cavity and centrally directed processes that enter the forebrain. Members of all classes of gnathostomes have been found to possess a terminal nerve, some components of which demonstrate immunoreactivity to the peptides Phe-Met-Arg-Phe-NH2 (FMRFamide) and gonadotropin-releasing hormone (GnRH). To explore the possibility that lampreys possess a terminal nerve, we examined the distribution of these peptides in the silver lamprey, Ichthyomyzon unicuspis, by using antisera to FMRFamide and to four forms of GnRH. We found cells with FMRFamide-like immunoreactivity in the preoptic area and the isthmal gray region of the mesencephalon, and found labeled fibers throughout the preoptic-infundibular region. Occasional labeled fibers were scattered through many regions of the brain, including the optic nerve and olfactory bulb; however, unlike species that possess a terminal nerve, lampreys have no immunoreactive cells or fibers in the olfactory nerve or nasal epithelia. In addition, we observed GnRH-immunoreactive cell bodies in the preoptic area of all animals and in the ventral hypothalamus of one individual. Most of the labeled fibers extended ventrally to the hypothalamus, with other fibers extending throughout the striatum and hypothalamic-neurohypophyseal region. A few fibers in other regions, including the optic nerve, were also labeled; we detected no immunoreactivity in the olfactory bulb, olfactory nerve, or nasal epithelia. The use of different GnRH antisera resulted in remarkably similar patterns of labeling of both cells and fibers. In summary, we did not observe either GnRH or FMRFamide-like immunoreactivity in the olfactory regions that represent the typical path of terminal nerve fibers, nor were we able to locate a terminal nerve ganglion. We conclude that lampreys may lack a terminal nerve, and that the previously described fiber bundle extending from the nasal sac to the ventral forebrain may constitute an extra-bulbar olfactory pathway.
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PMID:Silver lampreys (Ichthyomyzon unicuspis) lack a gonadotropin-releasing hormone- and FMRFamide-immunoreactive terminal nerve. 880 28

The present study investigated the effect of central administration of the prostaglandin of E2 type (PGE2) on the distribution of the immediate early gene (IEG) c-fos mRNA and the transcriptional activity of corticotropin-releasing factor (CRF) and its type 1 receptor in the brain of conscious rats. Adult male rats were sacrificed 30 min and 2 h after a single infusion of PGE2 into the right lateral ventricle (2 micrograms/10 microliters) and their brains cut from the olfactory bulb to the end of the medulla in 30 micrometer coronal sections. mRNAs encoding the IEG c-fos and CRF1 receptor were assayed by in situ hybridization histochemistry using 35S-labeled exonic riboprobes whereas the primary transcript (heteronuclear (hn)RNA) for CRF was detected using intronic probe technology as an index of CRF transcriptional activity. Colocalization of c-fos mRNA within CRF, vasopressin (AVP), and oxytocin (OT) neurons was determined by means of a combination of immunocytochemistry and in situ hybridization techniques on the same brain sections. Thirty min after PGE2 injection, a moderate to strong positive signal for c-fos mRNA was detected in multiple structures of the brain such as the medial preoptic area/organum vasculosum of the lamina terminalis, supraoptic nucleus (SON), parvocellular and magnocellular divisions of the paraventricular nucleus (PVN) of the hypothalamus, central nucleus of the amygdala, nucleus of the solitary tract, dorsal motor nucleus of the vagus, area postrema, dorsal division of the ambiguus nucleus, and throughout the choroid plexus and leptomeninges. A smaller but significant c-fos expression was observed in various structures including the subfornical organ, bed nucleus of the stria terminalis, arcuate nucleus, and periventricular nucleus of the hypothalamus. Two h after treatment with the PG, the signal for c-fos mRNA in most of these brain nuclei vanished. In the parvocellular nucleus of the PVN, c-fos was expressed in CRF-immunoreactive (ir) and OT-ir neurons, whereas in the magnocellular part of that nucleus and in the SON, this transcript was essentially colocalized in OT-ir neurons. Activation of CRF neuroendocrine cells was also associated with an increase in CRF transcription as revealed by the selective presence of CRF primary transcript (hnRNA), which was stimulated only in the PVN but not in any other nuclei in the brains of PGE2-treated rats. Central administration of PGE2 also induced expression of the CRF type 1 receptor in the parvocellular PVN. Taken together, these results provide clear anatomical evidence that central PGE2 injection causes specific and selective expression of c-fos in several brain structures recognized to be activated in the brains of endotoxin-challenged rats. It is therefore possible that PG of E2 type plays a crucial role within the CNS in the interface between the immune and nervous systems to modulate neuroendocrine responses, such as the hypothalamic-pituitary-adrenal axis.
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PMID:C-fos mRNA pattern and corticotropin-releasing factor neuronal activity throughout the brain of rats injected centrally with a prostaglandin of E2 type. 889 25

This study has investigated the effect of stimulating the region of origin of the mesolimbic dopaminergic system, the ventral tegmental area (VTA), with the substance P analogue DiMe-C7 on the regional expression of c-fos in the rat forebrain. We have previously shown this treatment produced a prolonged increase in blood pressure and heart rate which was mediated by both dopaminergic mechanisms and vasopressin release. Stimulation of the VTA resulted in increased levels of c-Fos immunostaining in several target regions of the mesolimbic dopaminergic system (such as the frontal cortex, olfactory tubercle, islands of Calleja and amygdala), with the notable exception of the nucleus accumbens. A marked increase in c-fos expression was also found in the supraoptic nucleus but not the paraventricular nucleus in the hypothalamus. These results support a role for a number of target areas of the mesolimbic dopaminergic system and vasopressin release in the increase in blood pressure and heart rate produced by stimulation of the VTA.
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PMID:Regional expression of c-fos in rat brain following stimulation of the ventral tegmental area. 897 38

In the ewe, [Arg8]vasopressin (AVP) release into the olfactory bulb (OB) modulates transmitter release necessary for the induction of olfactory memory. [3H]AVP binding to a microsomal preparation of ovine OB revealed saturable binding to a single class of high affinity sites (Kd = 2.03 +/- 0.18 nM). The density of binding sites was significantly greater in the lamb than ewe, but did not vary across the adult oestrous cycle. Displacement using AVP analogues showed that their relative affinities for the ovine V1a receptor were identical to the rat hepatic V1a receptor. These data demonstrate a single class of AVP binding sites in the ovine OB and the first pharmacological characterisation of the ovine V1a receptor.
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PMID:Characterisation of vasopressin V1a binding sites in the ovine olfactory bulb. 897 42


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