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)

An immunocytochemical analysis with 33 antisera was undertaken to investigate the localization of 25 different neurotransmitter-related antigens in the hypothalamic suprachiasmatic nucleus in the rat. To obtain estimates of relative densities of immunoreactive axons a stereological approach was used involving counting of intersections of immunoreactive axons with a superimposed semi-circle test grid. All neurotransmitter-related antigens found in perikarya within the suprachiasmatic nucleus, including those stained with antisera against bombesin, gastrin-releasing peptide, neurophysin, vasopressin, somatostatin, gamma-aminobutyrate, glutamate decarboxylase and vasoactive intestinal polypeptide were also found in axons within the nucleus. A greater number of these immunoreactive axons was found within the nucleus than in the adjacent anterior hypothalamus. The size of all immunoreactive axons in the suprachiasmatic nucleus was consistently small; immunoreactive axons were found ramifying widely in the nucleus, often ending with terminal boutons near perikarya immunoreactive for the same antigen. All neurotransmitter-related substances found in perikarya of the suprachiasmatic nucleus were also found in axons crossing over the midline to innervate the contralateral nucleus, providing an anatomical substrate for a high degree of communication between the paired nuclei. Axons immunoreactive for other putative transmitters including serotonin arising outside the nucleus were also found in high densities within the nucleus and crossing over the midline between the nuclei. Immunoreactivity for some transmitters was found in axons of similar densities within and outside the nucleus, including antisera against tyrosine hydroxylase; a small number of dopamine beta-hydroxylase and a few phenylethanolamine N-methyltransferase-immunoreactive axons were found in the SCN, suggesting that dopamine, norepinephrine and epinephrine may occur in a limited number of axons in the nucleus. Small numbers of axons immunoreactive with antisera raised against cholecystokinin, prolactin, substance P, thyrotropin-releasing hormone and choline acetyltransferase were found within the suprachiasmatic nucleus. Axons immunoreactive for luteinizing hormone-releasing hormone, adrenocorticotropic hormone, alpha-melanocyte-stimulating hormone and neurotensin were rarely found within the suprachiasmatic nucleus; axons immunoreactive for luteinizing hormone-releasing hormone, adrenocorticotropic hormone, cholecystokinin and tyrosine hydroxylase were found in both horizontal and coronal sections in the area between the left and right suprachiasmatic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurotransmitters of the hypothalamic suprachiasmatic nucleus: immunocytochemical analysis of 25 neuronal antigens. 241 88

An ultrastructural immunocytochemical study was undertaken to identify neuroactive substances contained in presynaptic boutons in the hypothalamic suprachiasmatic nucleus. Axonal boutons containing immunoreactive gamma-aminobutyrate, glutamate decarboxylase, neurophysin/vasopressin, gastrin releasing peptide/bombesin, somatostatin and serotonin were localized within the hypothalamic suprachiasmatic nucleus with pre-embedding peroxidase immunostaining. Synaptic contacts were found between boutons containing each of these substances and postsynaptic structures. While some variation in synaptic morphology existed, most of the immunoreactive contacts were of the symmetrical type. Previous work has indicated that neuroactive peptides may be found in highest concentrations in dense-core vesicles, to examine the subcellular localization of the amino acid inhibitory transmitter gamma-aminobutyrate, ultrastructural immunocytochemistry with pre-embedding peroxidase was compared with post-embedding immunocytochemistry with colloidal gold. Ultracryothin sections were also used for ultrastructural localization of gamma-aminobutyrate and glutamate decarboxylase immunoreactivity. Both gamma-aminobutyrate and glutamate decarboxylase immunoreactivity were found throughout the cytoplasm of immunoreactive boutons when pre-embedding peroxidase was used; with post-embedding colloidal gold immunostaining, label was found over areas containing small clear vesicles, and over mitochondria of immunoreactive axons. At the dilutions used in this study, strongly immunoreactive gamma-aminobutyrate dendrites, boutons forming asymmetrical synapses, and cell bodies were not found. Differences between pre-embedding and post-embedding immunostaining may be due to antigen and label diffusion caused by mild fixation and membrane damage necessary for antisera penetration during pre-embedding immunostaining. These results suggest that gamma-aminobutyrate, gastrin releasing peptide, somatostatin and vasopressin are contained in axons making contact with neurons of the suprachiasmatic nucleus, and may function as neurotransmitters here. Since all of these substances can also be localized in perikarya within the suprachiasmatic nucleus, there is a strong possibility that at least some of the axons containing immunoreactivity for each of these substances may be involved in local circuit interactions between neurons within the suprachiasmatic nucleus.
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PMID:Gamma-aminobutyrate, gastrin releasing peptide, serotonin, somatostatin, and vasopressin: ultrastructural immunocytochemical localization in presynaptic axons in the suprachiasmatic nucleus. 242 91

The hypothalamus receives neuronal afferents from numerous sources including inputs from limbic structures, such as the amygdala and hippocampus, and from brainstem regions involved in the regulation of the cardiovascular system and other autonomic functions. These afferents using a vast array of neurotransmitters and neuropeptides influence the activity of the hypothalamic neurons which synthesize and secrete the hypothalamic releasing and release-inhibiting factors into the hypophyseal portal circulatory system. The afferents can modulate the activity of the hypothalamic neurons by forming synapses on the neuronal cell body, on the nerve terminals in the median eminence or both. The chemicals most frequently used as neurotransmitters are the biogenic amines, including the catecholamines (norepinephrine, dopamine and epinephrine), serotonin, acetylcholine and gamma-aminobutyric acid (GABA). The stimulatory influence of norepinephrine, serotonin, and acetylcholine on the secretion of corticotropin (ACTH) in rodents and man will be discussed, whereas GABA exerts an inhibitory effect on the secretion of ACTH in both man and rodents. These effects appear to be mediated by changes in the secretion of the corticotropin-releasing hormone (CRH) and vasopressin into the hypophyseal portal circulation. Numerous neuropeptides appear to alter the secretion of ACTH in the rat. We will discuss the stimulatory actions of neuropeptide Y (NPY), angiotensin II, and peptides of immune cell origin on the secretion of ACTH and CRH. The opioid peptides inhibit the secretion of CRH into the portal blood, however, they exert a potent stimulatory effect on prolactin secretion in the rat and man.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pituitary gland: neuropeptides, neurotransmitters and growth factors. 257 Nov 83

Discrete brain structures were analysed for gamma-aminobutyric acid (GABA) and vasopressin content in normo- and hypotensive rats treated with the glutamic acid decarboxylase inhibitor, 3-mercaptopropionic acid (MPA) and the GABAA agonist muscimol. In the normotensive group treated with MPA only, the concentration of vasopressin increased in the supraoptic nucleus, indicating an inhibitory role for GABA. In the hypotensive group a rise in the vasopressin level in the nucleus of the solitary tract was detected and the GABA level decreased in the supraoptic nucleus. Muscimol decreased the concentration of vasopressin in the nucleus of the solitary tract. The changes in the concentration of vasopressin may be a result of increased or decreased activation of the GABAergic system. The results show that the GABA- and vasopressinergic systems somehow interact although the more precise way of action remains to be clarified.
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PMID:Biochemical evidence for the GABA regulation of vasopressin levels in microdissected brain structures after servo-controlled hypotension. 278 40

In conscious rats, intracerebroventricular (i.c.v.) injections of gamma-aminobutyric acid (GABA), a GABA-uptake inhibitor (nipecotic acid), and artificial CSF (aCSF) were restricted to forebrain regions and their effect on baroreceptor-mediated arginine-vasopressin (AVP) release was studied. AVP release was stimulated by the hypotension resulting from combined treatment with a converting enzyme inhibitor (CEI) and chlorisondamine (CHLOR), a ganglionic blocking agent. CEI + CHLOR reduced mean arterial pressure (MAP) from 118 +/- 2 to 63 +/- 2 mm Hg, but pressure then rose to a compensated level of 78 +/- 1 mm Hg. The compensation in MAP was shown to be AVP-dependent at the end of the experiment since the vascular AVP antagonist, d(CH2)5Tyr(Me)AVP, reduced MAP from 78 +/- 1 to 63 +/- 1 mm Hg. While AVP was contributing to MAP maintenance, GABA (15, 50 and 150 micrograms) caused dose-related reductions in MAP (5 +/- 1.7 +/- 1 and 11 +/- 2 mm Hg, respectively). Nipecotic acid (3-350 micrograms) also caused dose-related reductions in MAP (from 3 +/- 1 to 15 +/- 2 mm Hg), while aCSF had no effect on MAP. Pretreatment with d(CH2)5Tyr(Me)AVP, antagonized completely the depressor effects of GABA and nipecotic acid. In other rats, blood samples were taken to measure the changes in plasma AVP concentrations (pAVP) induced by CEI + CHLOR and subsequent treatment with aCSF or nipecotic acid (175 micrograms). Hypotension induced by CEI + CHLOR caused a significant increase in pAVP. Forebrain-restricted nipecotic acid significantly suppressed pAVP (61 +/- 8% reduction; P less than 0.05 vs aCSF). These data provide evidence of an endogenous forebrain GABAergic system which, when activated, can inhibit baroreceptor-mediated AVP release.
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PMID:Evidence of an endogenous forebrain GABAergic system capable of inhibiting baroreceptor-mediated vasopressin release. 280 69

A new strategy was devised for the targeted immobilization of ligands on aminohexyl- and carboxyhexyl-agarose. Selectively protected neurotransmitter amino acids and neuropeptides were coupled to amino or carboxyl group-containing agarose derivatives using activated esters, mixed anhydrides or carbodiimides. After coupling, agarose beads were dehydrated and the protecting groups were cleaved in non-aqueous media with acids (trifluoroacetic acid, formic acid). Agarose beads were rehydrated and applied for affinity chromatography and cell surface recognition. The same compounds were coupled to derivatized polyacrylamide beads containing primary amino (Acrylex A), acyl hydrazide (Acrylex AH-100) or carboxyl (Acrylex C-100) groups. Protecting groups were removed by acidolytic cleavage. Oxytocin, vasopressin, tetra- and pentagastrin, cholecystokinin, leucine-enkephalin and carboxyl-bearing derivatives of the neurotransmitters noradrenaline, dopamine, histamine, serotonin, acetylcholine and gamma-aminobutyric acid were immunobilized on agarose and on derivatized polyacrylamide gels.
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PMID:Targeted immobilization of neurotransmitters and neuropeptides on agarose and on Acrylex polymers. 287 23

Picrotoxin, a gamma-aminobutyric acid (GABA) antagonist, administered to spinal rats elicited dose-related increases in mean blood pressure and circulating plasma vasopressin concentration which were found to be highly correlated (r = 0.952; P less than .001) 6 min after infusion of picrotoxin. Pretreatment with the vasopressin antagonist d(CH2)5Tyr(Me)arginine vasopressin (10 microgram/kg i.v.) blocked the picrotoxin-induced pressor response. Administration of bicuculline (1.0 mg/kg i.v.), a second GABA antagonist, caused an increase in mean blood pressure and plasma vasopressin, whereas strychnine, another central nervous system stimulant thought not to act via a GABAergic mechanism, failed to evoke a significant change in either mean blood pressure or plasma vasopressin. Midcollicular decerebration decreased base-line plasma vasopressin concentrations and also prevented the picrotoxin-induced increase in pressure and vasopressin. The data from this study suggest that blockade of tonic GABAergic inhibition by GABA antagonists causes the release of vasopressin into the systemic circulation which results in a pressor response in spinal rats. The level at which this GABAergic inhibition occurs is not known; however, the GABA antagonists appear to require an intact supraspinal neuraxis to cause the release of vasopressin from the neurohypophysis.
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PMID:Stimulation of vasopressin release by gamma-aminobutyric acid antagonists in spinal cord transected rats. 299 98

In vivo extracellular recordings from rat supraoptic and paraventricular magnocellular neurosecretory cells (MNCs) indicate that putative vasopressin-secreting MNCs may be identified by an abrupt and brief cessation in firing consequent to a transient drug-induced rise in arterial pressure sufficient to activate arterial baroreceptors. In the diagonal band of Broca (DBB), a population of neurons projecting towards the supraoptic nucleus are activated during this drug-induced hypertension. Electrical stimulation in DBB selectively depresses supraoptic vasopressin-secreting MNCs. Intracellular recordings in perfused hypothalamic explants confirm a DBB-evoked bicuculline-sensitive and chloride-dependent postsynaptic inhibition, similar to that associated with the application of gamma-aminobutyric acid (GABA) in approximately half of supraoptic MNCs. Since bicuculline also selectively blocks baroreceptor-induced inhibition in supraoptic MNCs, it is proposed that the depressant baroreflex input to vasopressin-secreting MNCs involves a population of DBB neurons and GABAergic interneurons located close to MNCs. An excitatory and selective input to vasopressin-secreting MNCs follows chemoreceptor activation, possibly mediated by the A1 noradrenergic cell group in the ventrolateral medulla. Another excitatory input to both vasopressin- and oxytocin-secreting MNCs is triggered by circulating angiotensin II and appears to be relayed centrally through an angiotensinergic projection from the subfornical organ.
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PMID:Cardiovascular input to hypothalamic neurosecretory neurons. 304 23

A pharmaco-histochemical method for demonstrating the enzyme 4-aminobutyrate: 2-oxoglutarate transaminase was applied to the sections of the rat supraoptic nucleus region. The reactions of GABAergic interneurons and their relationship to neurosecretory neurons were studied. Medium-sized neurons heavily stained for transaminase were detected in the perinuclear zone just dorsal to the supraoptic nucleus. Neurons within the supraoptic nucleus were not stained. However, the perikarya of some neurosecretory neurons in the dorsal region of the supraoptic nucleus, as well as in discrete groups scattered throughout the nucleus; were surrounded by the granular reaction products. The results strongly suggest that these strongly positive neurons in the perinuclear zone send axons to the supraoptic nucleus, where they richly divide into many branches, which synapse on the perikarya of some vasopressin and oxytocin cells.
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PMID:4-aminobutyrate: 2-oxoglutarate transaminase-containing neurons in the perinuclear zone of the rat supraoptic nucleus. 309 48

Antisera specific for gamma-aminobutyric acid (GABA) or its biosynthetic enzyme, glutamate decarboxylase, were used in pre- and postembedding immunocytochemical techniques at the light and electron microscopic levels, to visualize the GABAergic innervation of the hypothalamic supraoptic nucleus. Immunostaining for glutamate decarboxylase or gamma-aminobutyric acid were also combined with oxytocin and vasopressin immunolocalization, thereby permitting evaluation of the contribution of the innervation onto each type of neuron in this nucleus. Light microscopy of semithin plastic sections or vibratome slices stained for glutamate decarboxylase or gamma-aminobutyric acid, with peroxidase-antiperoxidase as immunolabel, revealed an extensive punctate labeling in the supraoptic nucleus and its immediate surroundings. Quantitative analysis of glutamate decarboxylase immunostaining in semithin sections indicated a comparable density of immunopositive punctae at the anterior and posterior levels of the nucleus (14-27 X 10(6) per mm3 tissue). Glutamate decarboxylase- or gamma-aminobutyric acid-immunoreactive cell bodies were never observed within the nucleus although they were detected in the hypothalamus immediately dorsolateral to the nucleus. Electron microscopy of vibratome slices treated with antiglutamate decarboxylase or antigamma-aminobutyric acid and peroxidase-antiperoxidase, or of ultrathin sections stained directly with antigamma-aminobutyric acid and immunoglobulin-coupled colloidal gold, showed that the immuno-reactive punctae represented, in the main, axonal terminals. They invariably contained small, rounded clear vesicles and, at times, one or two larger, dense cored vesicles; they all formed symmetrical synapses onto magnocellular cell bodies and dendrites. Oxytocin and vasopressin neurons were contacted in a similar fashion by glutamate decarboxylase- or gamma-aminobutyric acid-positive boutons in semithin sections of the nucleus stained simultaneously for glutamate decarboxylase and oxytocin and in ultrathin sections stained for glutamate decarboxylase or gamma-aminobutyric acid and oxytocin or vasopressin. Glutamate decarboxylase- or gamma-aminobutyric acid-positive terminals often formed synapses onto two postsynaptic elements in the same plane of section ("double" synapses), a synaptic configuration usually encountered in supraoptic nuclei of lactating animals. In such cases, the postsynaptic somata were oxytocinergic.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunocytochemical analysis of the GABAergic innervation of oxytocin- and vasopressin-secreting neurons in the rat supraoptic nucleus. 353 41


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