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)

Antibodies directed against the neurotransmitter gamma-aminobutyric acid (GABA) enabled the ultrastructural localization of GABA in conventional glutaraldehyde fixed and osmium postfixed material of the rat supraoptic nucleus and neural lobe. GABA was visualized using immunogold postembedding staining in axonal profiles that terminate on dendrites, axons or cell bodies throughout the supraoptic nucleus. The optimum ultrastructural preservation made possible the visualization of GABA terminals, also in the neural lobe. Here GABA axons were found to terminate synaptically on pituicytes and axonal profiles containing large dense core vesicles. These results emphasize, from an anatomical point of view, the potency of GABA to influence, as a transmitter, the release of vasopressin and oxytocin, both at the level of the cell body and of the neural lobe.
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PMID:Ultrastructural localization of GABA in the supraoptic nucleus and neural lobe. 356 67

The GABAergic innervation of the goldfish pituitary was studied at the light and electron microscope levels by means of radioautography after in vitro incubation in tritiated gamma-aminobutyric acid (GABA) and immunocytochemistry using antibodies against GABA. Following incubation of pituitary fragments in a medium containing tritiated GABA, a selective uptake of the tracer was observed within the digitations of the neurohypophysis. Silver grain clusters were also observed in the adenohypophyseal tissue. At the electron microscope level, this uptake was found to correspond to nerve endings containing small clear and dense-core vesicles. These labeled profiles were located mainly in neurohypophyseal digitations in close apposition with the basement membrane separating the neurohypophysis from the adenohypophysis. However, they were also encountered in direct contact with most adenohypophyseal cell types in the different lobes. These results were confirmed by immunocytochemical data demonstrating the presence of numerous GABA immunoreactive fibers in both anterior and neurointermediate lobes. They were found either in the digitations of the neurohypophysis or in the adenohypophysis in direct contact with the glandular cells with a distribution and an ultrastructural aspect similar to those observed by radioautography. These data demonstrate that the pituitary of teleosts receives a massive GABAergic innervation. Although physiological data providing a functional significance for such an innervation are lacking, the present study suggests that, as already documented in mammals, GABA may be involved in the neuroendocrine regulation of pituitary functions in teleosts.
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PMID:Central GABAergic innervation of the pituitary in goldfish: a radioautographic and immunocytochemical study at the electron microscope level. 366 9

To study the morphological substrate for interaction between two chemically distinct neuronal types, two double ultrastructural immunolabeling strategies were employed. In the first, two different electron-dense markers were used to examine simultaneously two different neurotransmitter-related antigens in the hypothalamic supraoptic nucleus in the same thin section. Results obtained with the first method were confirmed with a second approach based on postembedding immunostaining of alternate serial thin sections with different antisera. Antiserum against glutamate decarboxylase, the enzyme responsible for the synthesis of the inhibitory amino acid transmitter gamma-aminobutyric acid (GABA), or antisera against GABA, was used to localize immunoreactive axons in the hypothalamic supraoptic nucleus. With light microscopy, glutamate decarboxylase- and GABA-immunoreactive axon terminals immunostained with peroxidase were found arborizing throughout all areas of the nucleus; terminal boutons were found adjacent to unlabeled somata within the nucleus. Cells containing immunoreactive oxytocin, vasopressin, and neurophysin were localized with peroxidase. Glutamate decarboxylase-immunoreactive axons stained with peroxidase prior to embedding in plastic were demonstrated to contact neurons which contained vesicles immunostained with neurophysin antiserum by a post-embedding immunocytochemical procedure which used immunoglobulins or protein A adsorbed to colloidal gold as a second ultrastructural marker. Quantitative evaluation of post-embedding staining with colloidal gold using a neurophysin primary antiserum indicated a specific antigen localization in neurosecretory vesicles. A critical factor in this double-labeling paradigm was that immunological reagents used in the second series did not cross-react with those used in the first series, regardless of the species of origin of antisera. To provide further verification of GABAergic synapses on neurophysin-containing neurons, alternate serial ultrathin sections were stained with colloidal gold using antisera against either neurophysin or GABA; boutons immunoreactive for GABA made synaptic contact with supraoptic neurons containing neurophysin immunoreactivity. Converging results obtained with these two procedures indicate that GABAergic axons synapse directly on neurons containing oxytocin or vasopressin in the rat hypothalamic supraoptic nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Dual ultrastructural localization of two neurotransmitter-related antigens: colloidal gold-labeled neurophysin-immunoreactive supraoptic neurons receive peroxidase-labeled glutamate decarboxylase- or gold-labeled GABA-immunoreactive synapses. 390 66

Previous studies have shown that hypotension produced by drugs facilitating gamma-aminobutyric acid (GABA) transmission was caused by a decrease in sympathetic nervous system outflow. We attempted to determine if GABA agonists and GABA uptake inhibitors could also lower arterial pressure that was elevated by increasing the secretion of endogenous vasopressin. GABA and nipecotic acid, an uptake inhibitor of GABA, were administered intraventricularly to determine the cardiovascular effects of these agents in nephrectomized rats made acutely hypertensive with hypertonic saline. A 2-hr i.v. infusion of hypertonic saline (3.0 mEq/ml) increased arterial pressure from 119 +/- 2 to 157 +/- 2 mm Hg. Intraventricular administration of artificial cerebrospinal fluid, 100 micrograms of GABA and 175 micrograms of nipecotic acid produced a peak decrease in blood pressure of 0 +/- 0, 30 +/- 4 and 22 +/- 3 mm Hg, respectively. In nephrectomized rats receiving an equal volume of isotonic saline (0.15 mEq/ml), infused i.v. arterial pressure did not change. In these animals, central infusions of artificial cerebrospinal fluid, 100 micrograms of GABA and 175 micrograms of nipecotic acid decreased blood pressure only 1 +/- 1, 13 +/- 2 and 8 +/- 3 mm Hg, respectively. Further experiments utilizing nephrectomized rats infused with hypertonic saline were designed to determine the mechanism for the augmented depressor response produced by these agents. Elimination of the contribution of vasopressin to arterial pressure with a vascular vasopressin antagonist reduced the depressor responses produced by 100 micrograms of GABA and 175 micrograms of nipecotic acid to 10 +/- 3 and 8 +/- 3 mm Hg, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:GABAergic inhibition of hypertonic saline-induced vasopressin-dependent hypertension. 400 86

The inhibition of gamma-aminobutyric acid (GABA) synthesis did not interfere with the suppressive effect of dexamethasone on the stress-induced rise of plasma corticosterone levels in vasopressin-deficient homozygous Brattleboro rats. In dexamethasone-treated heterozygous rats corticosterone and vasopressin secretion increased after stress provided GABA synthesis was inhibited. The results indicate that inhibition of corticotrophin secretion by corticosteroids may in part be mediated by enhancement of GABA synthesis and a consequent inhibition of vasopressin release.
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PMID:Vasopressin secretion as a possible target of the gamma-aminobutyric acid-mediated component of the corticosteroid feedback effect. 406 85

Among the biochemical theories proposed for schizophrenia the best-founded appears to be the dopaminergic theory. Dopaminergic agonists exacerbate schizophrenic symptoms. Neuroleptics, which are the most effective drugs in schizophrenia, are dopaminergic-blocking agents. Other biochemical disorders have been demonstrated in some cases of schizophrenia but results are not always consonant. The presence of abnormal compounds, i.e. methylated derivatives or phenylethylamine, has often been mentioned. Several disorders of enzymes have also been reported, such as a defect in beta-dopamine hydroxylase or an abnormal activity of the MAO which metabolizes the indolamines and catecholamines. Disorders of the metabolism of noradrenaline and serotonin have also been suggested, mainly on experimental evidence. Other compounds have been incriminated, such as endorphins, gamma-aminobutyric acid, lysine-8 vasopressin or prostaglandins. The action of neuroleptics can be ascribed to dopaminergic respector blockade, as a safe approximation. However, the demonstration of several dopaminergic pathways and of several types of receptors makes the understanding of their mode of action all the more difficult that they interplay with many other neurotransmittors.
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PMID:[Biochemistry of schizophrenia and mechanism of action of neuroleptics]. 613 Jun 4

When rats were injected with 6-hydroxydopamine the catecholaminergic nerve terminals in their intermediate lobes exhibited distinct signs of degeneration. Morphometric examination of the Golgi apparatus in cells of the intermediate lobe of these rats showed significant enlargement of Golgi cisternae. The release of adrenocorticotropin, beta-endorphin/lipotropin and alpha-melanotropin from intermediate-lobe cells in vitro was measured by radioimmunoassay. The high basal peptide release was inhibited by dopamine and stimulated by methyl-isobutyl-xanthine. In contrast, gamma-aminobutyric acid, serotonin, histamine and noradrenaline, or corticotropin-releasing hormone, rat hypothalamic extract and vasopressin had no or only very weak effects. These observations indicate that the synthetic apparatus of intermediate-lobe cells is constantly depressed by dopaminergic nerves. We were not able to stimulate peptide release from intermediate-lobe cells by use of the above-mentioned endogenous agents.
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PMID:Control of peptide release from cells of the intermediate lobe of the rat pituitary. 614 94

Neurons of the lower brain stem maintain resting levels of arterial pressure (AP), mediate reflex responses from cardiopulmonary receptors, and are an important site of the hypotensive actions of alpha 2-adrenergic agonists. Details of the pathways and transmitters that mediate tonic and reflex control of AP are emerging. Afferent fibers of cardiopulmonary receptors in the ninth and tenth nerves terminate bilaterally in the nucleus of the tractus solitarius (NTS). Although some neurons contain substance P, the primary neurotransmitter appears to be the excitatory amino acid L-glutamate (L-glu). Neurons in rostral ventrolateral medulla, which most probably comprise the C1 group of epinephrine neurons, are also critical in AP control. C1 neurons project to innervate cholinergic preganglionic sympathetic neurons in the spinal cord. Stimulation of the C1 area electrically or with L-glu increases AP, while lesions or local injection of the inhibitory amino acid gamma-aminobutyric acid (GABA) lowers AP to levels comparable to spinal cord transection. Lesions of C1 neurons or their pathways abolish vasodepressor reflexes from baroreceptors and vagal afferents. In contrast, noradrenergic neurons of the caudal ventrolateral medulla, the A1 group, project rostrally to innervate, in part, vasopressin neurons of the hypothalamus. Stimulation of A1 neurons lowers AP, while lesions or GABA elevates it. We propose that C1 neurons comprise the so-called tonic vasomotor center of the brain stem and also mediate, via a projection from the NTS, the vasodepressor limb of baroreflexes. The NTS-C1 projection may be GABAergic.
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PMID:Brain stem catecholamine mechanisms in tonic and reflex control of blood pressure. 615 1

1 In cats anaesthetized with pentobarbitone sodium or chloralose, the amino acids, gamma-aminobutyric acid (GABA) and glycine, were applied to the ventral surface of the brain through paired Perspex rings placed across the medulla. 2 Applied to a region situated at the transition between medulla and cord, both amino acids greatly attenuated and even abolished the vasopressin release in response to carotid occlusion. Glycine was about 100 times more potent than GABA and effective in a concentration of 0.1 mg/ml. The pressor response to carotid occlusion was not affected. 3 Applied to a region situated 5 to 6 mm more rostrally, the amino acids did not affect vasopressin release but in strong concentrations, greatly attenuated the pressor response to carotid occlusion. 4 The two responses to carotid occlusion, vasopressin release and the pressor response, can thus be influenced independently. 5 It is concluded that the pathways carrying afferent impulses from the baroreceptors in the carotid sinus reach the ventral surface of the brain stem at two regions. At both, synaptic transmission can be blocked by the application of an inhibitory amino acid and thus prevent either the release of vasopressin at the caudal site, or the increase of vasomotor tone at the rostral site.
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PMID:Inhibition of vasopressin release to carotid occlusion by gamma-aminobutyric acid and glycine. 626 64

Cultured endothelial cells derived from cerebral microvessels separated from 2-day-old rat brain contain a specific beta 2 and alpha 2-adrenergic sensitive adenylate cyclase (AC). Among the various tested hormones, PGE1 and PGE2 were found to be the most potent activators, while adenosine, angiotensin I and II, gamma-aminobutyric acid and vasoactive intestinal peptide inhibited the enzyme activity. However, acetylcholine, histamine, serotonin, glycine, glutamine, bradykinin, neurotensin and vasopressin (Lysine and Arginine) had no effect on the adenylate cyclase activity in this model. The susceptibility of the cerebrovascular endothelial AC system to the vasoactive substances as well as presence of beta 2 and alpha 2-type adrenergic receptors in the cultured endothelium provides additional support for the proposed endothelial involvement in the regulation of cerebrovascular permeability and blood flow.
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PMID:Cerebral endothelial cell culture. I. The presence of beta 2 and alpha 2-adrenergic receptors linked to adenylate cyclase activity. 627 96


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