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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A small conductance K+ channel was identified in smooth muscle cells of the rat aortic cell line A7r5 and also in rat aortic smooth muscle cells in primary culture, using conventional single-channel recording techniques. The single-channel conductance shows no rectification, either in the range -70 to +40 mV under asymmetrical conditions (9.1 pS), or in the range -100 to +50 mV in symmetrical 150 mM K+ (37 pS). Channel activity is reversibly inhibited by extracellular application of charybdotoxin, with a concentration of 8 nM producing half-maximal inhibition. It is unaffected by apamin or scyllatoxin. Channel activity depends on the presence of free Ca2+ on the cytosolic face of the membrane, with an activation zone between 0.1 and 1 microM. This small-conductance, charybdotoxin-sensitive, Ca(2+)-regulated K+ channel is activated by vasoconstrictors such as vasopressin and endothelin.
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PMID:A small-conductance charybdotoxin-sensitive, apamin-resistant Ca(2+)-activated K+ channel in aortic smooth muscle cells (A7r5 line and primary culture). 137 76

Opioid peptide- as well as vasopressin-containing neurons synapse on gonadotropin releasing hormone neurons in juvenile macaques. In this study we performed double-label immunostaining for opioid and vasopressin neurons in the paraventricular and supraoptic nuclei in order to assess their interrelationships. Neuroendocrine neurons in the hypothalamus were prelabeled by microinjection of electron-dense retrograde tracer into the median eminence, and were easily identified in frontal Vibratome sections. Sections through the paraventricular and supraoptic nuclei were immunostained for vasopressin with the peroxidase-antiperoxidase technique, and for opioids using the indirect immunogold method. By light microscopy, opioid-immunoreactive inputs appeared to innervate an average of 39% of the vasopressin neurons in the paraventricular nucleus and 33% in the supraoptic nucleus, and were more prevalent anteriorly. Clusters of opioid afferents formed cup-like calices around major processes of many vasopressin neurons, especially in the paraventricular nucleus. Electron microscopy revealed that these groups of opioid axon terminals made frequent symmetrical and fewer asymmetrical synapses on both neuroendocrine and non-neuroendocrine vasopressinergic cell bodies and dendrites. Our study did not reveal vasopressin-opioid synapses in these hypothalamic nuclei, but this does not preclude the possibility of their existence elsewhere. These results indicate that opioid afferents modulate vasopressin neuronal activity in the monkey paraventricular and supraoptic nuclei. Previous results have suggested that corticotropin releasing hormone acts via vasopressinergic neurons to stimulate opioid neuronal activity and to inhibit gonadotropin releasing hormone release. Taken together, the data suggest that stressful stimuli could initiate a series of neuropeptidergic interactions which ultimately alter pulsatile gonadotropin releasing hormone secretion and thus gonadotropin secretion in primates.
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PMID:Opioid synapses on vasopressin neurons in the paraventricular and supraoptic nuclei of juvenile monkeys. 177 44

These experiments were designed to test the thesis that prostaglandins produced by the cortical collecting tubule cells could modulate the vasopressin-induced osmotic water permeability (Pf). The dose-response curve for vasopressin-sensitive Pf showed the Km to be 1 microU ml-1. Exogenous PGE2 and PGF2 alpha (0.1 microM) inhibited the Pf induced by 1 microU ml-1 vasopressin when they were present in the bath solution. PGE2 (0.1 microM) in the lumen failed to inhibit the normal vasopressin-induced Pf, thus indicating an asymmetrical effect. Exposure of the tubule to 10 microM meclofenamate following stimulation of Pf by 0.2, 1.0, 10, or 100 microU ml-1 vasopressin failed to further increase the Pf. Pretreatment with meclofenamate or arachidonic acid (AA) failed to produce a different Pf response from controls. Neither naproxen (10 microM) nor AA altered significantly the Pf induced by 1 microU ml-1 vasopressin while methylisobutylxanthine, as expected, significantly enhanced Pf. The stable endoperoxide analogs U-44069 and U-46619, which mimic the actions of thromboxane A2 in many systems and which can stimulate osmotic water flow in the toad bladder, had no effect on Pf. Acidifying the lumen to pH 5.2 enhanced the Pf induced by 1 microU ml-1 vasopressin but subsequent exposure to meclofenamate did not cause an additional increment. These experiments demonstrate that exogenous prostaglandins are effective only from the basolateral surface of the cortical collecting tubule; that endogenous prostaglandins, if produced by these epithelial cells, do not produce demonstrable effects on vasopressin-sensitive Pf; and that endogenously produced thromboxane is not the likely reason for these results. Finally, the cortical collecting tubule response to many factors modulating Pf is considerably different from salientian urinary bladders.
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PMID:Modulation of vasopressin-induced water permeability of the cortical collecting tubule by endogenous and exogenous prostaglandins. 241 98

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

GABAergic neuronal profiles in the supraoptic nucleus of the rat were immunohistochemically identified by using a purified GABA antibody with the peroxidase-antiperoxidase method. The localization of GABA-like immunoreactivity in nerve terminals on the neurosecretory neurons was examined electron microscopically. A few small GABAergic neurons were found inside the supraoptic nucleus while only a very few medium-sized ones were detected in the perinuclear zone. Intrinsic, non-GABAergic small neurons covered by GABAergic neuropil were also detected. The neuropil with GABAergic axo-somatic synapses evenly encompassed unlabeled neurosecretory perikarya throughout the supraoptic nucleus. The GABAergic system seems to inhibit both vasopressin and oxytocin cells. In this area, glia cells showed clear outlines of unlabeled somata around counter-stained nuclei. Blood capillaries in the supraoptic nucleus were only slightly covered with a GABAergic neuropil. Electron microscopic observations demonstrated the presence of GABAergic axo-somatic symmetrical and axo-dendritic asymmetrical synapses on the neurosecretory neurons. GABA-like immunoreactivity was localized on the membranes of microtubules and synaptic vesicles, on the external membranes of the mitochondria, and on the inner leaf of the presynaptic sites. Numerous pairs of non-immunoreactive synapses were arranged along these immunoreactive synapses.
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PMID:Immunohistochemical studies on the GABAergic system in the rat supraoptic nucleus using the PAP method with an application of electron microscopy. 355 72

This paper reports a theoretical analysis of osmotic transients and an experimental evaluation both of rapid time resolution of lumen to bath osmosis and of bidirectional steady-state osmosis in isolated rabbit cortical collecting tubules exposed to antidiuretic hormone (ADH). For the case of a membrane in series with unstirred layers, there may be considerable differences between initial and steady-state osmotic flows (i.e., the osmotic transient phenomenon), because the solute concentrations at the interfaces between membrane and unstirred layers may vary with time. A numerical solution of the equation of continuity provided a means for computing these time-dependent values, and, accordingly, the variation of osmotic flow with time for a given set of parameters including: P(f) (cm s(-1)), the osmotic water permeability coefficient, the bulk phase solute concentrations, the unstirred layer thickness on either side of the membrane, and the fractional areas available for volume flow in the unstirred layers. The analyses provide a quantitative frame of reference for evaluating osmotic transients observed in epithelia in series with asymmetrical unstirred layers and indicate that, for such epithelia, P(f) determinations from steady-state osmotic flows may result in gross underestimates of osmotic water permeability. In earlier studies, we suggested that the discrepancy between the ADH-dependent values of P(f) and P(DDw) (cm s(-1), diffusional water permeability coefficient) was the consequence of cellular constraints to diffusion. In the present experiments, no transients were detectable 20-30 s after initiating ADH-dependent lumen to bath osmosis; and steady-state ADH-dependent osmotic flows from bath to lumen and lumen to bath were linear and symmetrical. An evaluation of these data in terms of the analytical model indicates: First, cellular constraints to diffusion in cortical collecting tubules could be rationalized in terms of a 25-fold reduction in the area of the cell layer available for water transport, possibly due in part to transcellular shunting of osmotic flow; and second, such cellular constraints resulted in relatively small, approximately 15%, underestimates of P(f).
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PMID:Osmosis in cortical collecting tubules. A theoretical and experimental analysis of the osmotic transient phenomenon. 484 67

The ultrastructure of the vasopressin neurons of the paraventricular nucleus of the hypothalamus was studied by immunocytochemical techniques. Tissue antigen was detected in unembedded tissue sections using a monoclonal antibody that recognizes vasopressin but not oxytocin or vasotocin. At the light-microscopic level, reaction product was seen to fill the cytoplasm of the neuron cell body as well as large portions of the dendrite and axon. Immunoreactive spines were seen on both somatic and dendritic surfaces and their presence was confirmed at the ultrastructural level. In the light-microscope, axonal processes do not have spines and are thinner and more varicose than dendritic processes. At the electron-microscopic level, both axons and dendrites of the vasopressin cells are filled with reactive neurosecretory granules. The presence of large numbers of these organelles made it difficult to distinguish proximal dendrites from Herring bodies (axonal swellings). At the ultrastructural level, reaction product was also observed in the cytoplasm of all segments of the vasopressin cells. The presence of reaction product outside of membranous compartments is undoubtably due to disruption of membranes by detergent treatment or exposure to basic pH. However, the staining procedure used did allow us to examine the synaptic input to the vasopressin cells. All portions of the vasopressin neuron receive a diverse innervation. The somata have synapses on their surfaces and on spines. These axo-somatic terminals are primarily, but not exclusively, symmetrical and the presynaptic elements contain spherical or elongate vesicles. On the dendrites, terminals again were observed on the surface or on spines. these axo-dendritic synapses were usually asymmetrical. The presynaptic elements contained clear spherical, elongate or pleomorphic vesicles. Occasional varicosities with dense-core granules were seen to make en passant contacts with dendrites; these contacts did not have obvious membrane specializations. Input to vasopressin axons was studied both along the paraventricular-neurohypophysial tract and in the median eminence. Vasopressin axons receive a synaptic input (axo-axonic), predominately of the asymmetric variety with clear, spherical vesicles in the presynaptic element. These findings demonstrate that the vasopressin neurons of the paraventricular nucleus receive a diverse innervation.
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PMID:Ultrastructural studies of vasopressin neurons of the paraventricular nucleus of the hypothalamus using a monoclonal antibody to vasopressin: analysis of synaptic input. 687 93

On the basis of current knowledge of neuroanatomy and our previous research with cardiac vagal tone, we have proposed the vagal circuit of emotion regulation. The vagal circuit of emotion regulation incorporates lateral brain function with the regulation of the peripheral autonomic nervous system in the expression of emotion. The vagus and the vagal circuit do not function independently of other neurophysiological and neuroendocrine systems. Research on brain activity (see Dawson, in this volume; Fox, in this volume) and research on adrenocortical activity (see Stansbury & Gunnar, in this volume) demonstrate that EEG and cortisol are related to emotion states and to individual differences similar to those that we have investigated. The vagal circuit emphasizes not only the vagus but also the lateralization of specific brain structures in emotion regulation. The emphasis of the vagal circuit on right-brain-stem structures stimulates several testable hypotheses regarding the function of specific structures in the right brain in emotion regulation. These speculations are consistent with other reports (see Dawson, in this volume; Fox, in this volume) describing asymmetrical EEG activity during expressed emotions. Moreover, the vagal circuit does not exist independently of the brain structures and peptide systems regulating cortisol (see Stansbury & Gunnar, in this volume). Areas in the brain stem regulating vagal activity are also sensitive to the peptides that regulate cortisol (e.g., vasopressin and corticotropin-releasing hormone). In this essay, we have provided information regarding the relation between vagal tone and emotion regulation. A review of research indicates that baseline levels of cardiac vagal tone and vagal tone reactivity abilities are associated with behavioral measures of reactivity, the expression of emotion, and self-regulation skills. Thus, we propose that cardiac vagal tone can serve as an index of emotion regulation. Historically, the vagus and other components of the parasympathetic nervous system have not been incorporated in theories of emotion. Recent developments in methodology have enabled us to define and accurately quantify cardiac vagal tone. Theories relating the parasympathetic nervous system to the expression and regulation of emotion are now being tested in several laboratories.
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PMID:Vagal tone and the physiological regulation of emotion. 798 59

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71

The effects of intra-amniotic administration of 1-desamino-8-D-arginine-vasopressin (DDAVP) at 14 days of embryogenesis on movement asymmetry in neonatal and mature mongrel white rats were studied. Controls consisted of intact and sham-operated animals, as well as rats given intra-amniotic saline. The population profile of asymmetry was assessed in terms of the tail position of rats aged two days, and also in terms of the direction of excursions in a T-maze in three-months males. The proportion of animals showing asymmetrical tail poses was no more than 36% in controls; the ratio of left-asymmetrical and right-asymmetrical intact rats was 2:1. DDAVP increased the number of rats with asymmetrical tail poses by a factor of 1.5-2.6, and right-asymmetrical individuals became predominant. This effect was demonstrated graphically as a bell-shaped dose-response curve with a peak response at doses of 3 x 10(-8) and 3 x 10(-6) mg. The selection probability for the right-hand side of the maze in experimental animals was 0.71 +/- 0.06, which was significantly higher than in animals of the three control groups, which showed no preference for the direction of excursions. These results indicate lateralization of the action of DDAVP in the developing central nervous system, leading to a predominance of right-sided motor responses in neonatal and mature rats.
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PMID:Population profile of brain asymmetry in rats after intra-amniotic administration of vasopressin. 919 68


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