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

Binding sites for oxytocin (OXT) and alpha-melanocyte-stimulating hormone (alpha-MSH) in brain of homozygous Brattleboro rats were immunocytochemically visualized after ventricular administration of the peptides by Accurel implants. Two patterns were found: 'ring type' staining in perineuronal structures was observed in CA1 and CA3 areas of ventral hippocampus and in subiculum for OXT implanted brains and a very weak staining in striatum for alpha-MSH-implanted brains; cytoplasmic staining of intracellular binding sites was observed in the bed nucleus of the stria terminalis (BST) in brains with OXT implants and in the anterodorsal thalamic nucleus (AD) and postcingulate cortex in brains with alpha-MSH implants. These localizations are different from those described for vasopressin binding sites in the same rat strain.
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PMID:Immunocytochemically stained binding sites for oxytocin and alpha-melanocyte-stimulating hormone in rat brain following ventricular administration. 242 69

1. Magnocellular neurosecretory cells (MNCs) were impaled in the supraoptic nucleus of rat hypothalamic explants maintained in vitro. Current- and voltage-clamp analysis of the osmotically induced response was performed at 34 degrees C. 2. Addition of mannitol or NaCl to cause a rise in fluid osmolarity (greater than +6 mosM) caused a membrane depolarization whose amplitude increased when elicited from more hyperpolarized levels. Changes in temperature (34-28 degrees C), addition of TTX, or superfusion with Na(+)-free or Ca2(+)-free solutions did not block the osmotically induced depolarization. In control solutions the response was consistently accompanied by an increase in the frequency of spontaneous postsynaptic potentials. Thus, osmotic stimuli have a direct effect on MNCs, and they also apparently activate other neurones which are presynaptic to these cells. 3. Under voltage-clamp, hyperosmotic stimuli induced an inward current (Io) accompanied by an increase in membrane conductance. The current was unaffected or slightly enhanced by doubling the external K+ concentration. Io was also characterized by a linear I-V relation (between -100 and -50mV) and an extrapolated reversal potential near -10 mV. Io presumably results from the activation of a voltage-independent and non-selective cationic conductance. 4. Hyperosmotic stimuli did not affect the depolarizing after-current (IDAP) responsible for the production of phasic bursts. However, the inward shift of the post-spike I-V curve caused by Io could reduce or eliminate the region of net outward current which lies negative to spike threshold in silent neurones. Thus in MNCs displaying IDAP, activation of Io by a rise in osmotic pressure can induce or enhance phasic bursting activity. 5. Application of hyperosmotic stimuli sufficient to excite most MNCs (+20 to +80 mosM) did not elicit a response from any of seventeen neurones impaled in areas lateral and caudal to the supraoptic nucleus. Recordings obtained from three CA1 neurones in slices of rat hippocampus revealed that stimuli in excess of +100 mosM are required to evoke appreciable non-specific depolarizations. 6. These studies indicate that the specific endogenous osmosensitivity of MNCs results from the activation of the intrinsic current Io. Furthermore, interactions between Io and IDAP explain how osmotic stimuli can lead to the induction of phasic bursting activity, a response which is known to potentiate the secretion of vasopressin from the neural lobe.
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PMID:Ionic basis for the intrinsic activation of rat supraoptic neurones by hyperosmotic stimuli. 262 93

An immunocytochemical procedure was developed to localize binding sites for vasopressin (VP) in the brain of Brattleboro (di/di) rats after 2 weeks of continuous ventricular administration of the peptide. Accurel-polypropylene tubing loaded with 0.15, 1.5 or 15 micrograms vasopressin was implanted into the lateral ventricle. Subsequently, bound VP was detected immunocytochemically in 2 distinct patterns: in perineuronal structures and dots between cells, in the lateral septum (dorsorostral part), striatum, cingulate cortex, granular cells of the dentate gyrus of the hippocampus, pyramidal cells of CA1 and CA3 hippocampal areas and around cerebellar Purkinje cells. The high dose (15 micrograms) loaded implants revealed the most intense staining; in the cytoplasm of neuronal cell bodies in the lateral and medial septum, striatum, cingulate cortex, bed nucleus of the stria terminalis, organum vasculosum of the laminae terminalis and locus coeruleus. The most intense staining in cell bodies was observed in brains which had low-loaded implants (0.15-1.5 microgram). A variety of controls, proved that no aspecific uptake was involved in the present procedure. The distribution of VP binding sites was only partly coincident with known sites of VP fiber innervation, and largely agrees with data obtained by autoradiographic techniques for [3H]VP binding. The present immunocytochemical technique gave a higher resolution than the currently used autoradiographic techniques. The differences in pattern and intensity of staining due to increasing the dosage rate of the in vivo vasopressin treatment, might mean that the current procedure retains preferentially either low or high affinity populations of binding sites depending on the implanted dose.
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PMID:Immunocytochemically-stained vasopressin binding sites in rat brain. Ventricular application of vasopressin/Accurel in the Brattleboro rat. 354 Feb 18

Extracellular recordings from cells in the CA1b region of the in vitro hippocampal slice preparation demonstrate that bath-applied AVP (10(-6)-10(-12) M) frequently results in a decrease in the orthodromically evoked population spike amplitude. This suggests that AVP inhibits CA1 pyramidal cell firing in response to an orthodromic volley. This effect appears to be receptor-mediated, since a potent antagonist of the AVP V1 (vasopressor) receptor and a mixed oxytocin/vasopressin antagonist prevented the decrease in population spike amplitude observed in response to bath application of AVP. Hippocampal slices prepared from rats injected two days earlier with 1.0 micrograms AVP (intracerebroventricular) display increased sensitivity to the depressant effects of AVP at lower doses compared to controls. These results suggest that pretreatment of rats with AVP may alter the sensitivity of hippocampal cells to the depressant effects of this neuropeptide.
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PMID:Altered sensitivity to arginine vasopressin (AVP) in area CA1 of the hippocampal slice following pretreatment of rats with AVP. 367 73

Microinjection of oxytocin into the paraventricular nucleus of the hypothalamus or into the CA1 field of the hippocampus induced a dose-dependent increase in the number of penile erection and yawning episodes in male rats. The minimal effective dose of oxytocin injected into the paraventricular nucleus was 3 ng. This dose induced the above-mentioned behaviors in 60% of the treated rats. Doses of 9 ng or higher induced the symptomatology in more than 85% of the animals. On the other hand, when the peptide was injected into the CA1 field of the hippocampus, 9 ng bilaterally were necessary to elicit penile erection and yawning in 62% of the rats. Arg8-vasopressin, which only differs from oxytocin in two amino acids, induced penile erection and yawning when injected either into the paraventricular nucleus or into the hippocampus, but was 5-10 times less potent than oxytocin. Oxytocin injection into the lateral septum, caudate nucleus, subiculum, preoptic area, ventromedial nucleus and supraoptic nucleus, was ineffective. The powerful effect of oxytocin on the induction of yawning and penile erection, suggests a physiological role of hypothalamic and hippocampal oxytocin in the regulation of such responses.
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PMID:Oxytocin-induced penile erection and yawning: site of action in the brain. 380 3

The effects of arginine-vasopressin (AVP) on the excitability of 47 pyramidal cells of the CA1 region of the hippocampus were determined by using intracellular recording techniques in a submerged slice preparation. Addition of 10(-6) M AVP to the bathing medium evoked an increase in spike discharge which was slow in onset and only gradually reversible. The discharge was accompanied by an increase in excitatory postsynaptic potentials without significant change of the resting input resistance. AVP-induced excitation was found in 81% of ventral and 29% of dorsal hippocampal CA1 pyramidal cells. In low Ca2+, high Mg2+ solution this excitatory action by AVP was blocked. Microiontophoretic application of AVP onto apical or basal dendrites or the cell body did not result in excitation. These observations suggest that the action of AVP on CA1 pyramidal cells is transsynaptic and is more pronounced in ventral than dorsal CA1.
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PMID:Action of vasopressin on CA1 pyramidal neurons in rat hippocampal slices. 608 58

Oxytocin and vasopressin increased the rate of firing of a class of presumed non-pyramidal neurones located in the CA1 area of rat hippocampal slices. This excitatory effect persisted in conditions of synaptic uncoupling. In contrast, pyramidal neurones were either unaffected by neurohypophysial peptides or showed one or several of the following effects: a decrease in firing rate in cells which were spontaneously active; a slight membrane hyperpolarization; and an increase in the rate of occurrence of spontaneous inhibitory postsynaptic potentials. We therefore propose that oxytocin and vasopressin excite directly a class of non-pyramidal inhibitory interneurones, whereas their observed effect on pyramidal neurones is indirect and inhibitory.
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PMID:Contrasting effects of neurohypophysial peptides on pyramidal and non-pyramidal neurones in the rat hippocampus. 647 5

Neurohypophysial peptides were applied by superfusion to rat hippocampal slices. The peptides, arginine vasopressin, lysine vasopressin, arginine vasotocin and oxytocin, increased the activity of 88% of spontaneously active cells in the CA1 region and induced firing in many neurones that were not spontaneously active. The peptide sensitive cells appeared to be pyramidal cells rather than interneurones. The four peptides were found to be of roughly equivalent potency, producing a reversible, dose-dependent response in the range 10(-9) to 10(-6)M. Most of the cells were tested with more than one peptide and were always found to respond either to all or to none of them. The analogue [7-glycine]oxytocin and the deamino, dicarba derivatives of oxytocin and vasopressin were about as active as the parent compounds, but the oxytocin fragment prolyl-leucyl-glycinamide had no effect, and desglycinamide vasopressin was extremely weak. Responses to the peptides could be blocked by "specific" antagonists. The results suggest that all of the peptides are acting upon a single class of receptor.
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PMID:Neurohypophysial peptides and the hippocampus. II. Excitation of rat hippocampal neurones by oxytocin and vasopressin applied in vitro. 666 25

Vasopressin may be a neurotransmitter and in vivo experiments suggest that it acts on monoamine metabolism. The rat hippocampal slice contains serotonergic nerve terminals but not cell bodies; we studied the effect of vasopressin on the synthesis and release of serotonin from these nerve terminals during depolarization. Incubation of slices in a buffer containing 60 mM K+ (high K buffer) for 10 min stimulated the release of serotonin into bathing medium and resulted in a Ca2+-dependent depletion of tissue serotonin from about 4.2 to about 2.8 ng/mg of protein. Vasopressin (10(-7) M) inhibited this depletion by about 70% so that serotonin levels fell only to 3.8 ng/mg of protein. The peptide also augmented the high K+-induced release of serotonin into the bathing medium by about 60%. The synthesis of serotonin was measured by determining its accumulation during a period when its catabolism was inhibited by pargyline. Vasopressin augmented the synthesis of serotonin in slices incubated in high K buffer by about 60%. There are serotonergic nerve endings in both the dentate gyrus and CA1 regions of the hippocampus. The effect of vasopressin on tissue serotonin was confined to the dentate gyrus regions. The data show that vasopressin acts on a specific group of hippocampal nerve endings to increase serotonin synthesis. The resulting increase in tissue serotonin may be the factor leading to the observed increase in serotonin release.
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PMID:Vasopressin augments depolarization-induced release and synthesis of serotonin in hippocampal slices. 706 67

The distribution of cells expressing mRNA encoding a vasopressin V1a receptor (V1aR) was examined in Long-Evans male and female rats by in situ hybridization using a [35S]cRNA probe. Specific hybridization to the vasopressin V1aR mRNA was evident in cells of the frontal cortex, piriform cortex, internal granular layer and the medial, dorsal, ventral and lateral portion of the anterior olfactory nucleus, zona limitans of the islands of Calleja, suprachiasmatic nucleus, CA1, CA2, CA3 and dentate gyrus of the hippocampus, paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, arcuate nucleus, lateral habenular nucleus, and the molecular and granular cell layers of the cerebellum. The cerebellum, olfactory nucleus and the dentate gyrus appeared to be the most intensely labeled areas, while all other areas exhibited a lower level of expression. The anatomical distribution and the amount (as measured by optical density) of V1aR mRNA labeling was identical between male and female rats. This indicates that unlike the vasopressin gene itself, the expression of the vasopressin V1aR mRNA does not exhibit sexual dimorphism. These data demonstrate a wide spread distribution in the expression of the vasopressin V1aR mRNA in the CNS of male and female rats. This information on the anatomical distribution of the V1aR mRNA when combined with data concerning the anatomical distribution of the V1a binding sites, provides new information on the possible pre- and post-synaptic location of these neuropeptide receptors.
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PMID:Distribution of messenger RNA for the vasopressin V1a receptor in the CNS of male and female rats. 796 46


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