Substantia nigra osmoregulation: taurine and ATP involvement

2007 ◽  
Vol 292 (5) ◽  
pp. C1934-C1941 ◽  
Author(s):  
Ingrid Morales ◽  
Jose G. Dopico ◽  
Magdalena Sabate ◽  
Tomas Gonzalez-Hernandez ◽  
Manuel Rodriguez
Keyword(s):  
Substantia Nigra ◽  
Purinergic Receptors ◽  
Opposite Effect ◽  
Physiological Role ◽  
Disulfonic Acid ◽  
Microdialysis Probe ◽  
Inhibitory Neurotransmitter ◽  
Taurine Concentration ◽  
Dose Dependent

An extracellular nonsynaptic taurine pool of glial origin was recently reported in the substantia nigra (SN). There is previous evidence showing taurine as an inhibitory neurotransmitter in the SN, but the physiological role of this nonsynaptic pool of taurine has not been explored. By using microdialysis methods, we studied the action of local osmolarity on the nonsynaptic taurine pool in the SN of the rat. Hypoosmolar pulses (285-80 mosM) administered in the SN by the microdialysis probe increased extrasynaptic taurine in a dose-dependent way, a response that was counteracted by compensating osmolarity with choline. The opposite effect (taurine decrease) was observed when osmolarity was increased. Under basal conditions, the blockade of either the AMPA-kainate glutamate receptors with 6-cyano-7-nitroquinoxaline-2,3-dionine disodium or the purinergic receptors with pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid modified the taurine concentration, suggesting that both receptors modulate the extrasynaptic pool of taurine. In addition, these drugs decreased the taurine response to hypoosmolar pulses, suggesting roles for glutamatergic and purinergic receptors in the taurine response to osmolarity. The participation of purinergic receptors was also supported by the fact that ATP (which, under basal conditions, increased the extrasynaptic taurine in a dose-dependent way) administered in doses saturating purinergic receptors also decreased the taurine response to hypoosmolarity. Taken together, present data suggest osmoregulation as a role of the nonsynaptic taurine pool of the SN, a function that also involves glutamate and ATP and that could influence the nigral cell vulnerability in Parkinson's disease.

scholarly journals Modulation of crayfish retinal function by red pigment concentrating hormone

1995 ◽  
Vol 198 (7) ◽  
pp. 1447-1454 ◽  
Author(s):  
A Garfias ◽  
L Rodríguez-Sosa ◽  
H Aréchiga
Keyword(s):  
Circadian Rhythm ◽  
Light Adaptation ◽  
Retinal Pigment ◽  
Physiological Role ◽  
Pigment Cells ◽  
Red Pigment ◽  
Retinal Activity ◽  
Retinal Photoreceptors ◽  
Dose Dependent

The role of the crustacean octapeptide red pigment concentrating hormone (RPCH) in the control of crayfish retinal activity was explored. RPCH injection into intact animals resulted, after a latency of 10­30 min, in a dose-dependent enhancement of electroretinogram (ERG) amplitude lasting 60­120 min. RPCH was able to potentiate ERG amplitude in both light-adapted and dark-adapted animals. Following light-adaptation, responsiveness to RPCH was five times higher than following dark-adaptation. In conjunction with ERG enhancement, in light-adapted animals, RPCH injection elicited a dose-dependent retraction of distal retinal pigment, but did not affect proximal retinal pigment position. The effects of RPCH were blocked by a polyclonal antibody raised against a tyrosinated form of RPCH (A-tyr-RPCH). The antibody was also capable of partially blocking the nocturnal phase of the circadian rhythm of ERG amplitude and the darkness-induced retraction of distal retinal pigment. These results suggest that RPCH acts both on the retinal photoreceptors and on the distal pigment cells, playing a physiological role as a mediator of the effects induced by darkness and by the nocturnal phase of the circadian rhythm.

Altered β-adrenergic signal transduction in nonfailing hypertrophied myocytes from Dahl salt-sensitive rats

2000 ◽  
Vol 279 (5) ◽  
pp. H2502-H2508 ◽  
Author(s):  
Kohzo Nagata ◽  
Catherine Communal ◽  
Chee C. Lim ◽  
Mohit Jain ◽  
Thomas M. Suter ◽  
...  
Keyword(s):  
Ventricular Hypertrophy ◽  
Physiological Role ◽  
Cellular Level ◽  
Left Ventricular ◽  
Cell Shortening ◽  
Hypertrophied Myocardium ◽  
Intracellular Ca ◽  
Myocyte Contractility ◽  
Dose Dependent

Desensitization of the β-adrenergic receptor (β-AR) response is well documented in hypertrophied hearts. We investigated whether β-AR desensitization is also present at the cellular level in hypertrophied myocardium, as well as the physiological role of inhibitory G (Gi) proteins and the L-type Ca2+channel in mediating β-AR desensitization. Left ventricular (LV) myocytes were isolated from hypertrophied hearts of hypertensive Dahl salt-sensitive (DS) rats and nonhypertrophied hearts of normotensive salt-resistant (DR) rats. Cells were paced at a rate of 300 beats/min at 37°C, and myocyte contractility and intracellular Ca2+concentration ([Ca2+]i) were simultaneously measured. In response to increasing concentrations of isoproterenol, DR myocytes displayed a dose-dependent augmentation of cell shortening and the [Ca2+]i transient amplitude, whereas hypertrophied DS myocytes had a blunted response of both cell shortening and the [Ca2+]i transient amplitude. Interestingly, inhibition of Gi proteins did not restore β-AR desensitization in DS myocytes. The responses to increases in extracellular Ca2+ and an L-type Ca2+ channel agonist were also similar in both DS and DR myocytes. Isoproterenol-stimulated adenylyl cyclase activity, however, was blunted in hypertrophied myocytes. We concluded that compensated ventricular hypertrophy results in a blunted contractile response to β-AR stimulation, which is present at the cellular level and independent of alterations in inhibitory G proteins and the L-type Ca2+ channel.

Sulfate/oxalate exchange by lobster hepatopancreatic basolateral membrane vesicles

1995 ◽  
Vol 269 (3) ◽  
pp. R572-R577 ◽  
Author(s):  
G. A. Gerencser ◽  
M. A. Cattey ◽  
G. A. Ahearn
Keyword(s):  
Gradient Centrifugation ◽  
Basolateral Membrane ◽  
Physiological Role ◽  
Membrane Vesicles ◽  
Disulfonic Acid ◽  
Basolateral Membrane Vesicles ◽  
Sulfate Uptake ◽  
Discontinuous Sucrose Gradient ◽  
Carboxylic Anions

Purified basolateral membrane vesicles (BLMV) were prepared from lobster hepatopancreas by osmotic disruption and discontinuous sucrose gradient centrifugation. Radiolabeled sulfate uptake was stimulated by 10 mM intravesicular oxalate compared with gluconate-loaded vesicles. Sulfate/oxalate exchange was not affected by transmembrane valinomycin-induced potassium diffusion potentials (inside negative or inside positive), suggesting electroneutral anion transport. Sulfate uptake was not stimulated by the similar carboxylic anions formate, succinate, oxaloacetate, or ketoglutarate. Sulfate influx occurred by at least one saturable Michaelis-Menten carrier system [apparent Km = 6.0 +/- 1.7 mM; maximum flux (Jmax) = 382.3 +/- 37.0 pmol.mg protein-1 x 7 s-1]. Sulfate/oxalate exchange was significantly reduced by the anion antiport inhibitors 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid but was not affected by bumetanide or furosemide. The possible physiological role of this exchange mechanism in anion/sulfate transport across the crustacean hepatopancreas is discussed.

P2X purinoceptors in the feline pulmonary vascular bed: distribution and selective in vivo pharmacological probes

1996 ◽  
Vol 270 (6) ◽  
pp. L889-L897 ◽  
Author(s):  
C. F. Neely ◽  
I. Matot ◽  
V. K. Batra ◽  
X. Bo ◽  
G. Burnstock
Keyword(s):  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Physiological Role ◽  
Disulfonic Acid ◽  
Health And Disease ◽  
Alpha Beta ◽  
P2x Purinoceptor ◽  
Potent Vasoconstrictor ◽  
Dose Dependent

The distribution and identification of selective pharmacological probes for P2X purinoceptors in the pulmonary vascular (PV) bed of the cat have been investigated with autoradiographic and pharmacological techniques. Autoradiographic localization of the selective P2X purinoceptor ligand alpha, beta-[3H]methylene ATP (alpha, beta-MeATP) binding sites in cat lung shows that P2X purinoceptors are present in all vessels in the bed; high densities were present in large (2-mm diam) and small (0.5-mm diam) pulmonary arteries, bronchial arterioles (0.1-mm diam), and large pulmonary veins, whereas low density is characteristic of parenchymal arterioles and alveolar walls. Most of the binding is displaced with the P2X-purinoceptor agonist beta, gamma-methylene ATP and the putative selective P2X-purinoceptor antagonist pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid (PPADS) in all vessels; however, the binding is further displaced with the, P2Y-purinoceptor agonist 2-methylthio ATP (2-MeS-ATP), which suggests the presence of P2Y as well as P2X purinoceptors. P2X purinoceptors mediate potent vasoconstrictor actions in the PV bed. alpha, beta-MeATP is a selective agonist for P2X purinoceptors and does not act via serotonergic, histaminergic, adrenergic, or leukotriene vasoconstrictor receptors to produce an increase in PV resistance. The vasoconstrictor responses of alpha, beta-MeATP are attenuated by PPADS. However, PPADS has no effect on the vasodilation induced by ATP, adenosine, or 2-MeS-ATP. The diadenosine nucleotide AP5A also produced dose-dependent vasoconstrictor responses of the PV bed, which were approximately three times less potent than those of alpha, beta-MeATP and significantly reduced by PPADS. These data support that vasoconstrictor P2X purinoceptors are present on pulmonary vessels. The functional significance of these vascular P2X purinoceptors in the PV bed is not known; however, alpha, beta-MeATP, AP5A, and PPADS may be used in vivo to define their physiological role in health and disease in the lung.

scholarly journals Oligodendroglial GABAergic Signaling: More Than Inhibition!

2021 ◽  
Author(s):  
Xianshu Bai ◽  
Frank Kirchhoff ◽  
Anja Scheller
Keyword(s):  
Gaba Receptors ◽  
Gaba Receptor ◽  
Signal Transmission ◽  
Physiological Role ◽  
Inhibitory Neurotransmitter ◽  
Short Summary ◽  
Central Synapses ◽  
G Protein Coupled ◽  
Shed Light

AbstractGABA is the main inhibitory neurotransmitter in the CNS acting at two distinct types of receptor: ligand-gated ionotropic GABAA receptors and G protein-coupled metabotropic GABAB receptors, thus mediating fast and slow inhibition of excitability at central synapses. GABAergic signal transmission has been intensively studied in neurons in contrast to oligodendrocytes and their precursors (OPCs), although the latter express both types of GABA receptor. Recent studies focusing on interneuron myelination and interneuron-OPC synapses have shed light on the importance of GABA signaling in the oligodendrocyte lineage. In this review, we start with a short summary on GABA itself and neuronal GABAergic signaling. Then, we elaborate on the physiological role of GABA receptors within the oligodendrocyte lineage and conclude with a description of these receptors as putative targets in treatments of CNS diseases.

Regulation of breathing movements in fetal sheep by prostaglandin E2

1986 ◽  
Vol 60 (2) ◽  
pp. 526-531 ◽  
Author(s):  
L. D. Wallen ◽  
D. T. Murai ◽  
R. I. Clyman ◽  
C. H. Lee ◽  
F. E. Mauray ◽  
...  
Keyword(s):  
Low Voltage ◽  
Physiological Role ◽  
Fetal Sheep ◽  
Electrocortical Activity ◽  
Endogenous Prostaglandin ◽  
Pge2 Concentration ◽  
Regulation Of Breathing ◽  
Pg E2 ◽  
Dose Dependent

In fetal sheep, plasma prostaglandin (PG) E2 concentrations are high, and fetal breathing movements (FBM) occur intermittently, primarily during low-voltage fast electrocortical activity (LVFA). There is evidence suggesting that prostaglandins, specifically PGE2, may regulate FBM. To define the physiological role of PGE2 in regulation of FBM, we infused meclofenamate (0.9 mg X kg-1 X h-1), a prostaglandin synthetase inhibitor, into six fetal sheep to suppress endogenous prostaglandin production. Afterward, PGE2 was added in mean doses of 9, 18, 36, and 90 ng X kg-1 X min-1. Meclofenamate decreased PGE2 concentrations and increased FBM, especially during high-voltage slow electrocortical activity (HVSA). Addition of PGE2 reversed the effects of meclofenamate, increasing PGE2 concentrations and decreasing FBM, especially during HVSA. The response to PGE2 was dose dependent; the overall incidence of FBM and incidences of FBM during HVSA and LVFA were inversely correlated with both the infused PGE2 dose and the mean PGE2 concentration. At higher doses of PGE2, FBM occurred intermittently and only during LVFA; thus PGE2 infusion restored the physiological pattern of FBM. These results indicate that PGE2 regulates FBM by inhibiting FBM during HVSA.

Evidence for presence of functional beta-adrenoceptor in rabbit S2 proximal straight tubules

1991 ◽  
Vol 261 (3) ◽  
pp. F393-F399 ◽  
Author(s):  
K. Kudo ◽  
Y. Kondo ◽  
K. Abe ◽  
Y. Igarashi ◽  
K. Tada ◽  
...  
Keyword(s):  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
K Channel ◽  
Dependent Manner ◽  
Electrophysiological Properties ◽  
Beta Adrenoceptor ◽  
Organic Solute ◽  
Cell Depolarization ◽  
Dose Dependent

The effect of isoproterenol on the electrophysiological properties of the S2 proximal segment of the rabbit was examined. Isoproterenol at 10(-8) to 10(-4) M depolarized the basolateral membrane voltage (Vb) in a dose-dependent manner. Propranolol attenuated the isoproterenol-induced depolarization. These possible mechanisms of cell depolarization were explored. The role of luminal Na(+)-organic solute cotransport was negligible, since the removal of organic solute did not change the depolarization. Basolateral Na(+)-(HCO3-) cotransport was supported by the finding that 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid inhibited isoproterenol-induced depolarization. Basolateral K+ conductance was suggested by the finding that the application of Ba2+ blocked the isoproterenol-induced depolarization. Na(+)-K(+)-adenosine-triphosphatase (ATPase) was questionable. Although ouabain blocked isoproterenol-induced depolarization, the removal of Na+ did not inhibit the depolarization. Further experiment revealed that dibutylyl-adenosine 3',5'-cyclic monophosphate (cAMP), 8-bromo cAMP, and forskolin did not mimic the response of isoproterenol. These results demonstrate: 1) there is a functional beta-adrenoceptor that depolarizes Vb; 2) isoproterenol-induced depolarization is due to an inhibition of basolateral K+ channel or the activation of basolateral Na(+)-(HCO3-)n cotransport; 3) isoproteronol-induced depolarization is independent of cAMP in the rabbit proximal tubule.

scholarly journals TMEM16A calcium-activated chloride currents in supporting cells of the mouse olfactory epithelium

2019 ◽  
Vol 151 (7) ◽  
pp. 954-966 ◽  
Author(s):  
Tiago Henriques ◽  
Emilio Agostinelli ◽  
Andres Hernandez-Clavijo ◽  
Devendra Kumar Maurya ◽  
Jason R. Rock ◽  
...  
Keyword(s):  
Olfactory Epithelium ◽  
Olfactory System ◽  
Purinergic Receptors ◽  
Ion Selectivity ◽  
Ionic Composition ◽  
Physiological Role ◽  
Apical Surface ◽  
Supporting Cells ◽  
Sustentacular Cells

Glial-like supporting (or sustentacular) cells are important constituents of the olfactory epithelium that are involved in several physiological processes such as production of endocannabinoids, insulin, and ATP and regulation of the ionic composition of the mucus layer that covers the apical surface of the olfactory epithelium. Supporting cells express metabotropic P2Y purinergic receptors that generate ATP-induced Ca2+ signaling through the activation of a PLC-mediated cascade. Recently, we reported that a subpopulation of supporting cells expresses also the Ca2+-activated Cl− channel TMEM16A. Here, we sought to extend our understanding of a possible physiological role of this channel in the olfactory system by asking whether Ca2+ can activate Cl− currents mediated by TMEM16A. We use whole-cell patch-clamp analysis in slices of the olfactory epithelium to measure dose–response relations in the presence of various intracellular Ca2+ concentrations, ion selectivity, and blockage. We find that knockout of TMEM16A abolishes Ca2+-activated Cl− currents, demonstrating that TMEM16A is essential for these currents in supporting cells. Also, by using extracellular ATP as physiological stimuli, we found that the stimulation of purinergic receptors activates a large TMEM16A-dependent Cl− current, indicating a possible role of TMEM16A in ATP-mediated signaling. Altogether, our results establish that TMEM16A-mediated currents are functional in olfactory supporting cells and provide a foundation for future work investigating the precise physiological role of TMEM16A in the olfactory system.

Nitrergic and purinergic regulation of the rat pylorus

2000 ◽  
Vol 279 (4) ◽  
pp. G740-G747 ◽  
Author(s):  
Tadashi Ishiguchi ◽  
Toku Takahashi ◽  
Hidekazu Itoh ◽  
Chung Owyang
Keyword(s):  
Pyridoxal Phosphate ◽  
Disulfonic Acid ◽  
Dependent Manner ◽  
Field Stimulation ◽  
Inhibitory Effects ◽  
Reactive Blue 2 ◽  
Combined Administration ◽  
Dose Dependent ◽  
Nanc Relaxation

The role of nitric oxide (NO) and ATP in the regulation of nonadrenergic, noncholinergic (NANC) inhibitory transmission in the pylorus remains unclear. In the presence of atropine and guanethidine, electric field stimulation induced NANC relaxations in a frequency-dependent manner (1–20 Hz) in the rat pylorus. NANC relaxations were significantly inhibited by N G-nitro-l-arginine methyl ester (l-NAME; 10−4 M). P2Xpurinoceptor antagonist pyridoxal phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS; 3 × 10−5 M) and P2Y purinoceptor antagonist reactive blue 2 (2 × 10−5 M) had no effect on NANC relaxations. However, the combined administration of l-NAME and PPADS, but not reactive blue 2, evoked greater inhibitory effects on NANC relaxation than that evoked by l-NAME alone. α-Chymotrypsin and vasoactive intestinal polypeptide antagonist did not affect NANC relaxations. ATP (10−5–10−3 M) and P2Xpurinoceptor agonist α,β-methyleneadenosine 5′-triphosphate (10−7−10−5 M), but not P2Ypurinoceptor agonist 2-methylthioadenosine 5′-triphosphate (10−7−10−5 M), induced muscle relaxations in a dose-dependent manner, and relaxations were significantly reduced by PPADS and unaffected by TTX. These studies suggest that NO and ATP act in concert to mediate NANC relaxation of the rat pylorus. ATP-induced relaxation appears to be mediated by P2X purinoceptors located on smooth muscle cells.

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