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Voltage Dependent (voltage + dependent)
Selected AbstractsA role for the volume regulated anion channel in volume regulation in the murine CNS cell line, CADACTA PHYSIOLOGICA, Issue 2 2010V. L. Harvey Abstract Aim:, The role of the volume regulated anion channel (VRAC) in a model CNS neuronal cell line, CAD, was investigated. Methods:, Changes in cell volume following hypotonic challenges were measured using a video-imaging technique. The effect of the Cl, channel antagonists tamoxifen (10 ,m) and 4,4,-diisothiocyanatostilbene-2,2,-disulphonic acid (DIDS; 100 ,m) on regulatory volume decrease (RVD) were measured. The whole-cell voltage-clamp technique was used to characterize IClswell, the current underlying the VRAC. Results:, Using the video-imaging technique, CAD cells were found to swell and subsequently exhibit RVD when subjected to a sustained hypotonic challenge from 300 mOsmol kg,1 H2O to 210 mOsmol kg,1 H2O. In the presence of tamoxifen (10 ,m) or DIDS (100 ,m) RVD was abolished, suggesting a role for the VRAC. A hypotonic solution (230 mOsmol kg,1 H2O) evoked IClswell, an outwardly rectifying current displaying time-independent activation, which reversed upon return to isotonic conditions. The reversal potential (Erev) for IClswell was ,14.7 ± 1.4 mV, similar to the theoretical Erev for a selective Cl, conductance. IClswell was inhibited in the presence of DIDS (100 ,m) and tamoxifen (10 ,m), the DIDS inhibition being voltage dependent. Conclusions:, Osmotic swelling elicits an outwardly rectifying Cl, conductance in CAD cells. The IClswell observed in these cells is similar to that observed in other cells, and is likely to provide a pathway for the loss of Cl, which leads to water loss and RVD. As ischaemia, brain trauma, hypoxia and other brain pathologies can cause cell swelling, CAD cells represent a model cell line for the study of neuronal cell volume regulation. [source] Developmental changes in the modulation of respiratory rhythm generation by extracellular K+ in the isolated bullfrog brainstemDEVELOPMENTAL NEUROBIOLOGY, Issue 3 2003Rachel E. Winmill Abstract This study tested the hypothesis that voltage-dependent, respiratory-related activity in vitro, inferred from changes in [K+]o, changes during development in the amphibian brainstem. Respiratory-related neural activity was recorded from cranial nerve roots in isolated brainstem,spinal cord preparations from 7 premetamorphic tadpoles and 10 adults. Changes in fictive gill/lung activity in tadpoles and buccal/lung activity in adults were examined during superfusion with artificial CSF (aCSF) with [K+]o ranging from 1 to 12 mM (4 mM control). In tadpoles, both fictive gill burst frequency (fgill) and lung burst frequency (flung) were significantly dependent upon [K+]o (r2 > 0.75; p < 0.001) from 1 to 10 mM K+, and there was a strong correlation between fgill and flung (r2 = 0.65; p < 0.001). When [K+]o was raised to 12 mM, there was a reversible abolition of fictive breathing. In adults, fictive buccal frequency (fbuccal), was significantly dependent on [K+]o (r2 = 0.47; p < 0.001), but [K+]o had no effect on flung (p > 0.2), and there was no significant correlation between fbuccal and flung. These data suggest that the neural networks driving gill and lung burst activity in tadpoles may be strongly voltage modulated. In adults, buccal activity, the proposed remnant of gill ventilation in adults, also appears to be voltage dependent, but is not correlated with lung burst activity. These results suggest that lung burst activity in amphibians may shift from a "voltage-dependent" state to a "voltage-independent" state during development. This is consistent with the hypothesis that the fundamental mechanisms generating respiratory rhythm in the amphibian brainstem change during development. We hypothesize that lung respiratory rhythm generation in amphibians undergoes a developmental change from a pacemaker to network-driven process. © 2003 Wiley Periodicals, Inc. J Neurobiol 55: 278,287, 2003 [source] The Anticonvulsant SGB-017 (ADCI) Blocks Voltage-Gated Sodium Channels in Rat and Human Neurons: Comparison with CarbamazepineEPILEPSIA, Issue 3 2000Lucy Sun Summary: Purpose: SGB-017 (ADCI) is a novel anticonvul-sant that blocks both voltage-activated sodium channels and N -methyl- d -aspartate (NMDA)-receptor-gated channels. Results by Rogawski et al. suggested that SGB-017 produces its anticonvulsant action primarily by inhibition of NMDA-receptor channels. However, SGB-017 is effective in several animal models of epilepsy that are unresponsive to NMDA antagonists. These results indicate that block of NMDA-receptor channels is not the only mechanism contributing to its anticonvulsant activity. Thus the effects of SGB-017 on neu-ronal sodium channels were investigated. Methods: Whole cell voltage-clamp techniques were used to record sodium currents in freshly dissociated rat superior cervical ganglion (SCG) and hippocampal neurons and cultured human NT2 neurons. The effects of SGB-017 on the amplitude of sodium currents, elicited by a depolarizing pulse to 0 mV from different holding potentials, were measured and compared with those of carbamazepine (CBZ). Results: SGB-017 inhibited sodium currents in rat SCG and hippocampal neurons with a similar potency to CBZ. Like CBZ, the inhibition of sodium channels by SGB-017 was voltage dependent. Its median inhibitory concentration (IC50) for inhibition of sodium channels at depolarized holding potentials is similar to that for its inhibition of NMDA receptor channels. In human hNT2 neurons, SGB-017 was more potent than CBZ at inhibiting sodium currents. Conclusions: SGB-017 produces its anticonvulsant activity by blocking both sodium- and NMDA-receptor channels in a voltage- and use-dependent manner. The combination of these two mechanisms of action makes SGB-017 an effective AED in several different animal models of epilepsy. [source] Saturation and self-inhibition of rat hippocampal GABAA receptors at high GABA concentrationsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2002Katarzyna Mercik Abstract Current responses to ultrafast ,-aminobutyric acid (GABA) applications were recorded from excised patches in rat hippocampal neurons to study the gating properties of GABAA receptors at GABA concentrations close to saturating ones and higher. The amplitude of currents saturated at approximately 1 mm, while the onset rate of responses reached saturation at 4,6 mm GABA. At high GABA concentrations (> 10 mm), the amplitude of current responses was reduced in a dose-dependent manner with a half-blocking GABA concentration of approximately 50 mm. The peak reduction at high GABA doses was accompanied by a tendency to increase the steady-state to peak ratio. At concentrations higher than 30 mm, this effect took the form of a rebound current, i.e. during the prolonged GABA applications, the current firstly declined due to desensitization onset and then, instead of decreasing towards a steady-state value, clearly increased. Both the self-inhibition of GABAA receptors by high GABA doses and rebound were clearly voltage dependent, being larger at positive holding potentials. The fast desensitization component accelerated with depolarization at all saturating [GABA] tested. The rebound phenomenon indicates that the self-block of GABAA receptors is state dependent, and suggests that the sojourn in the desensitized conformation provides a ,rescue' from the block. We propose that high GABA concentrations inhibit the receptors by direct occlusion of the channel pore having no effect on the receptor gating. [source] High-frequency Impedance and Sensitivity of Micro-fluxgate Sensors Fabricated with Cobalt Base Amorphous FilmsIEEJ TRANSACTIONS ON ELECTRICAL AND ELECTRONIC ENGINEERING, Issue 4 2008Kwang-Ho Shin Non-member Abstract Micro-fluxgate sensors 2 mm long, 1.5 mm wide were fabricated with CoZrNb amorphous films. Their high-frequency input/output impedance was measured and evaluated to investigate whether the sensor output and/or sensitivity could be estimated by the complex impedance, especially the reactance. The output reactance changed from 11.1 to 6.1 ohm at 8 MHz by applying the external magnetic field of 10.5 Oe, whereas the input impedance changed from 12.3 to 10.1 ohm. The parasitic capacitance was driven from the measured reactance and resonance frequency. The inductance and inductive reactance could be evaluated with the parasitic capacitance and measured reactance. The tendency of output voltage dependent on frequency is similar to that of inductive reactance. The sensitivity of the fabricated sensor was 17.6 mV/VOe at 8 MHz. Copyright © 2008 Institute of Electrical Engineers of Japan. Published by John Wiley & Sons, Inc. [source] The AC Conductivity of Liquid-Phase-Sintered Silicon CarbideJOURNAL OF THE AMERICAN CERAMIC SOCIETY, Issue 8 2007Godfrey Sauti Analysis of the AC conductivity, complex dielectric constant, and the resulting immittance spectra of liquid-phase-sintered silicon carbide (SiC) ceramics showed that for this system, the dominant experimental observations are due to a multicomponent grain-boundary phase and not due to SiC grains. This is confirmed by noting that the temperature dependence of the conductivity of the components, derived from the impedance spectra, is proportional to exp[,(T0/T)1/4] and not to exp[,C/T]. The electrical properties of some of the grain boundaries are also found to be excitation voltage dependent. Combining the electrical results, which are also found to depend on the method of preparation and heat treatment, with a Rietveld analysis allows the composition of the grain boundaries of the models to be deduced. [source] Voltage-dependent and -independent titration of specific residues accounts for complex gating of a ClC chloride channel by extracellular protonsTHE JOURNAL OF PHYSIOLOGY, Issue 7 2009Marķa Isabel Niemeyer The ClC transport protein family comprises both Cl, ion channel and H+/Cl, and H+/NO3, exchanger members. Structural studies on a bacterial ClC transporter reveal a pore obstructed at its external opening by a glutamate side-chain which acts as a gate for Cl, passage and in addition serves as a staging post for H+ exchange. This same conserved glutamate acts as a gate to regulate Cl, flow in ClC channels. The activity of ClC-2, a genuine Cl, channel, has a biphasic response to extracellular pH with activation by moderate acidification followed by abrupt channel closure at pH values lower than ,7. We have now investigated the molecular basis of this complex gating behaviour. First, we identify a sensor that couples extracellular acidification to complete closure of the channel. This is extracellularly-facing histidine 532 at the N-terminus of transmembrane helix Q whose neutralisation leads to channel closure in a cooperative manner. We go on to show that acidification-dependent activation of ClC-2 is voltage dependent and probably mediated by protonation of pore gate glutamate 207. Intracellular Cl, acts as a voltage-independent modulator, as though regulating the pKa of the protonatable residue. Our results suggest that voltage dependence of ClC-2 is given by hyperpolarisation-dependent penetration of protons from the extracellular side to neutralise the glutamate gate deep within the channel, which allows Cl, efflux. This is reminiscent of a partial exchanger cycle, suggesting that the ClC-2 channel evolved from its transporter counterparts. [source] | ||||||||||