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)

1. Magnocellular neurosecretory cells (MNCs) were isolated from the supraoptic nucleus of adult Long-Evans rats using an enzymatic procedure. Immunocytochemical staining with antibodies against vasopressin and oxytocin revealed that MNCs can be identified by size. The membrane properties of these cells were examined at 32-34 degrees C using intracellular recording methods. 2. Isolated MNCs displayed a mean (+/- S.E.M.; n = 109) resting membrane potential of -64.1 +/- 1.0 mV, an input resistance of 571 +/- 34 M omega, and a time constant of 8.7 +/- 0.4 ms. Measurements of specific resistivity and input capacitance revealed that the soma of these cells accounts for a mere 20% of their total somato-dendritic membrane in situ. 3. Voltage-current relations measured near -60 mV were linear negative to spike threshold. From more hyperpolarized membrane potentials, voltage responses to depolarizing current steps displayed transient outward rectification and delayed impulse discharge. 4. Action potentials (76.6 +/- 0.9 mV) triggered from an apparent threshold of -59.3 +/- 0.1 mV broadened progressively at the onset of spontaneous or current-evoked spike trains. Steady-state spike duration increased as a logarithmic function of firing frequency with a maximum near 25 Hz. These effects were abolished in Ca(2+)-free solutions. 5. In all cells, evoked spike trains were followed by a prolonged Ca(2+)-sensitive after-hyperpolarization. In contrast, only a small proportion (16%) of MNCs displayed spontaneous bursting activity or depolarizing after-potentials following brief current-evoked bursts. 6. Isolated MNCs responded to amino acids (glutamate and GABA) and to the neuropeptide cholecystokinin, indicating that receptors for these neurotransmitters are expressed postsynaptically by MNCs and are retained following dissociation. 7. Increasing the osmolality of the superfusing solution by 5-30 mosmol kg-1 caused a membrane depolarization associated with a decrease of input resistance and accelerated spontaneous spike discharge in each of thirty-six MNCs tested. Current-clamp analysis suggested that these responses resulted from the activation of a cationic conductance. Excitatory effects of hyperosmolality were not observed in non-magnocellular neurones (n = 6).
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PMID:Properties of supraoptic magnocellular neurones isolated from the adult rat. 136 42

Pharmacologic investigations into the transmission processes underlying fictive swallowing in the rat have disclosed the potential diversity of chemical signals used in central deglutitive pathways. Monoaminergic mechanisms appear to serve as links between subcortical structures and the medullary pattern generator of swallowing (PGS), and may play a critical role in maintaining internal facilitatory drive, required by the PGS for optimal responsivity to peripheral sensory input. Cholinergic bulbar interneurons form an integral component of the PGS subnetwork controlling esophageal peristalsis. Local GABA neurons exert a tonic inhibition of the buccopharyngeal stage, may regulate buccopharyngeal-esophageal coupling, and may contribute to peristaltic rhythmic generation at both the premotoneuronal and motoneuronal level. Receptor subtypes for excitatory amino acids (glutamate, aspartate) are differentially associated with deglutitive premotoneurons for both the buccopharyngeal and esophageal stage, as well as with ambiguus motoneurons. Preliminary evidence suggests the existence of excitatory peptidergic mechanisms involving thyrotropin-releasing hormone, vasopressin, oxytocin, and somatostatin, a probable candidate for excitatory transmitter in the solitarioambigual internuncial projection to motoneurons innervating esophageal striated musculature. Further validation of this experimental model may ultimately help to establish a framework for the clinical recognition, management, and exploitation of drug actions on central deglutitive neuroeffectors.
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PMID:Neuropharmacologic correlates of deglutition: lessons from fictive swallowing. 168 Jun 8

Neurotransmitters including acetylcholine, dopamine, norepinephrine, serotonin, GABA and vasopressin were examined in control subjects and patients with Alzheimer-type dementia, involving presenile and senile dementia. Neurotransmitters exhibited various mode of changes with aging. Abnormalities found in senile or presenile dementia were not always parallel to the age-related changes. These results suggest that Alzheimer-type dementia cannot be understood as an accelerated senescence, but other etiological factors might be introduced for the manifestation of the dementia. Moreover, the disturbance in neurotransmitters revealed a difference between presenile Alzheimer's disease and senile dementia, indicating that further studies should be carried out taking the age of onset into consideration.
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PMID:Senile dementia and presenile dementia. 170 90

Arginine8-vasopressin (AVP, 10 micrograms), injected s.c., potentiated the motor-impairing effects of pentobarbital (10-20 mg/kg) injected i.p. in rats 1 h after AVP. Motor incoordination was assessed on the moving belt task. However, AVP (0.1-100 nM) failed to enhance pentobarbital potentiation of GABA-mediated 36Cl- uptake in rat cerebral cortical or cerebellar microsacs. There was also no effect of a 10 micrograms s.c. injection of AVP 1 h before killing, on pentobarbital potentiation of GABA-mediated chloride flux in either cerebral cortical or cerebellar microsacs.
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PMID:Arginine8-vasopressin potentiates the motor incoordinating effects of pentobarbital. 174 56

The recent investigations on biochemical and biophysical mechanisms of ethanol in acute intoxication, tolerance and physical dependence suggest that the cell membrane, intracellular metabolism and central neurotransmitters are involved. In acute intoxication ethanol increases the "fluidity" of the cell membrane and stimulates the central gabergic system. In alcoholics, the body adapts, and in the presence of ethanol, the cell membrane becomes more "rigid" and the gabergic system hypoactive. When alcohol intake is discontinued the hypoactivity of the gabergic system is unmasked and it is manifested as withdrawal syndrome. The alcohol intake compensates for the clinical symptoms of decreased gabergic activity and thereby continuously prevent the onset of withdrawal symptoms. On the other hand, intact central noradrenergic and 5-hydroxytryptaminergic systems as well as the neuropeptide vasopressin maintain the tolerance. After withdrawal syndrome, membrane alterations and the state of diminished gabergic activity gradually return to normal. This period of slow recuperation corresponds to the subacute withdrawal syndrome. In this period, there is a continuous desire for alcohol intake. Further, alcoholics, in this situation, are very vulnerable with feelings of insecurity, fragility and isolation. All these factors additionally induce a latent desire for ethanol. It follows then that a stimulation of decreased gabergic activity is a new approach in drug therapy of alcoholism. One of these new stimulants is acamprosate. The new substance is a structural analogue of GABA and acts as an agonist on gabergic receptors. Therefore, acamprosate improves the central gabergic activity. Alcoholics treated with acamprosate stated that they no longer felt a desire for alcohol intake. In this way, acamprosate maintains the abstinence for several months during the post-withdrawal phase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Modern drug therapy in alcoholism]. 180 68

The modulation of Ca2+ currents by neurotransmitters was studied in freshly dissociated rat spinal cord neurons, using the whole-cell patch-clamp technique. GABA, baclofen, adenosine, ATP, serotonin, norepinephrine, somatostatin, and dynorphin A inhibited the current through Ca2+ channels in a substantial fraction of cells, while substance P, vasoactive intestinal polypeptide, [D-ala2,d-leu5]-enkephalin, cholecystokinin-8 (sulfated), calcitonin gene-related peptide, angiotensin II, neurotensin, vasopressin, and thyrotropin-releasing hormone had no effect. In the case of baclofen, the inhibition is mediated, at least in part, by a GTP-binding protein. Suppression of Ca2+ current by neurotransmitters may represent a mechanism of presynaptic inhibition in the spinal cord.
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PMID:Neurotransmitter modulation of calcium current in rat spinal cord neurons. 196 36

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

The effects of vasoactive intestinal polypeptide (VIP), of a selective oxytocin antagonist and of GABA on basal and stimulated oxytocin and vasopressin release from isolated neurosecretory endings were investigated. Superfusion of the secretosomes with VIP (10(-7) M) induced an increased basal and stimulated release of both oxytocin and vasopressin. Addition of the oxytocin antagonist induced a decrease of the stimulated oxytocin release as compared to the control which indicated a positive feedback mechanism of oxytocin on oxytocin release. In presence of GABA (1 or 50 microM) no change in basal or stimulated oxytocin and vasopressin release was observed.
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PMID:Modulation of oxytocin and vasopressin release from rat neurosecretosomes: the roles of VIP oxytocin and GABA. 206 99

If we consider the chemical messengers in the central nervous system, there are about ten classic transmitters--the catecholamines, biogenic amines and amino acids--as opposed to over 50 different neuropeptides. These include previously well-established circulating hormones such as angiotensin, atrial natriuretic peptide, vasopressin and oxytocin, calcitonin and calcitonin gene related peptide (CGRP), the opioid family of peptides, gastrointestinal peptides, pituitary peptides and their releasing factors, and miscellaneous peptides such as the kinins, bombesin, gallanin, and others; all occur as neuropeptides in the brain. There is evidence supporting a role in central cardiovascular control for angiotensin, opioid peptides, substance P, neuropeptide Y, vasopressin, atrial natriuretic peptide, kinins, corticotropin releasing factor, bombesin, somatostatin, and some other peptides. They have been localized in brain areas known to be important for blood pressure regulation, and specific high-affinity peptide receptors have also been discovered. Upon central administration, these peptides produce cardiovascular effects, partly by interacting with other blood pressure-controlling neuroregulators, e.g. catecholamines and GABA. Central inhibition of brain peptide synthesis or interaction with competitive antagonists at the receptor site results in marked cardiovascular effects. Altered peptide levels and activity of synthesizing enzymes, as well as supersensitivity to the pressor action of some brain peptides, have been described in experimental models of hypertension. We are using angiotensin as a model peptide to study the peptidergic control of cardiovascular function.
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PMID:Peptidergic control of cardiovascular function: the angiotensin paradigm. 219 11

The coexistence of galanin (GAL)-like immunoreactivity (LI) with markers for catecholamines, 5-hydroxytryptamine (5-HT), GABA, or some neuropeptides was mapped in the rat CNS by using adjacent sections, as well as by elution-restaining and double-labeling immunocytochemistry. Many instances of coexistence were observed, but there were also numerous GAL-positive cell body populations displaying distributions similar to those of these markers but without apparent coexistence. In the hypothalamic arcuate nucleus GAL-LI was found in a large proportion of tyrosine hydroxylase (TH)-positive cell bodies (A12 cells), both in the dorsomedial and ventrolateral subdivisions, with a higher number in the latter. GAL-LI coexisted in glutamic acid decarboxylase (GAD)-positive somata in the posterior aspects of the arcuate nucleus and at all rostrocaudal levels in fibers in the external layer of the median eminence. In the anterior hypothalamus, a large population of the cells of the parvocellular and magnocellular paraventricular nuclei contained both GAL-LI and vasopressin-LI. Moreover, somata containing both GAD- and GAL-LI were seen lateral to the mammillary recess in the tuberal and caudal magnocellular nuclei. Some of the neurons of the caudal group were shown to project to the occipital cortex using combined retrograde tracing and immunofluorescence. With regard to mesencephalic and medullary catecholamine neurons, GAL-LI coexisted in a large proportion of the noradrenergic locus coeruleus somata (A6 cell group) and in the A4 group dorsolateral to the fourth ventricle, as well as in the caudal parts of the A2 group in the dorsal vagal complex. However, in more rostral parts of the latter, especially in the medial subdivision of the solitary tract nucleus, a very large population of GAL-IR small cell bodies was seen intermingling with catecholamine neurons, but they did not contain TH-LI. Furthermore, GAL-IR cell bodies coextensive with, but not coexisting in, TH-IR somata were seen in the C1 (epinephrine) horea in the ventrolateral medulla at the level of area postrema and in the most rostral aspects of the C1 group. Finally, 5-HT-positive cell bodies of the mesencephalic and medullary raphe nuclei and a subpopulation of coarse 5-HT nerve fibers in the hippocampus co-contained GAL-LI. The present results demonstrate that a GAL-like peptide is present in many systems containing other neuroactive compounds, including dopamine, norepinephrine, 5-HT, GABA, and vasopressin.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Coexistence of galanin-like immunoreactivity with catecholamines, 5-hydroxytryptamine, GABA and neuropeptides in the rat CNS. 243 3


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