Although the modulation of synaptic activity plays an important role in the modulation of neuronal excitability, the significance of the ambient modulation (AM) of neuronal excitability should be emphasized. The AM refers to the alterations of membrane potential of neuron resulted from distinct neural activities, such as the tonic inhibition and excitation through activation of extra-synaptic receptors, the paracrine actions of nearby neural and non-neural cells, endocrinal actions of blood borne hormones and other active chemical substances. The AM of neuronal excitability may have important bearings on distinct brain functions, such as the regulation and switching of cortical states, the appearance of chaotic and vague feelings, which are usually the characteristic features in many mental and neural disorders.
Membrane Potentials ; Neurons

BACKGROUND: Whereas sevoflurane (SEVO) has been reported to prolong the QT interval, little has been known on the electrophysiologic effects of SEVO which contributes to the prolongation of action potential (AP) duration. METHODS: The ventricular myocytes were obtained from enzymatically treated rat hearts. The standard whole cell voltage-clamp methods were used. The AP was measured using current clamp technique. As a repolarizing K+ current, the transient outward K+ current (I(to)), the sustained outward K+ current (I(sus)), and the inwardly rectifying K+ current (I(kI)) were measured. The L-type Ca2+ current (I(Ca), L) was also obtained. After the baseline measurements, the myocytes were exposed to 1.7 and 3.4% SEVO. SEVO concentrations in Tyrode superfusate at room temperature were 0.35 and 0.7 mM for 1.7 and 3.4% SEVO, respectively. Results are mean +/- SEM. RESULTS: SEVO prolonged the AP duration, while the amplitude and the resting membrane potential remained unchanged. At membrane potential of +60 mV, peak I(to) was significantly reduced by 18 +/- 2 and 24 +/- 2% by 0.35 and 0.7 mM SEVO, respectively. 0.7 mM SEVO did not shift the steady-state inactivation curve. Isus was unaffected by 0.7 mM SEVO. The I(kI) at -130 mV was little altered by 0.7 mM SEVO. I(Ca), L was significantly reduced by 28 +/- 3 and 33 +/- 1% by 0.35 and 0.7 mM SEVO, respectively. CONCLUSIONS: Prolongation of AP duration by SEVO in rat ventricular myocytes is likely to be caused by a reduction of I(to). Resting membrane potential was unaffected by SEVO, which seems to be related to no alteration of I(kI).
Action Potentials ; Animals ; Heart ; Membrane Potentials ; Muscle Cells* ; Rats*

No abstract available.
Doxorubicin* ; Membrane Potentials* ; Membranes* ; Papillary Muscles*

No abstract available.
Doxorubicin* ; Membrane Potentials* ; Membranes* ; Purkinje Fibers* ; Sodium*

Patch clamp is a technique that can measure weak current in the level of picoampere (pA). It has been widely used for cellular electrophysiological recording in fundamental medical researches, such as membrane potential and ion channel currents recording, etc. In order to obtain accurate measurement results, both the resistance and capacitance of the pipette are required to be compensated. Capacitance compensations are composed of slow and fast capacitance compensation. The slow compensation is determined by the lipid bilayer of cell membrane, and its magnitude usually ranges from a few picofarads (pF) to a few microfarads (μF), depending on the cell size. The fast capacitance is formed by the distributed capacitance of the glass pipette, wires and solution, mostly ranging in a few picofarads. After the pipette sucks the cells in the solution, the positions of the glass pipette and wire have been determined, and only taking once compensation for slow and fast capacitance will meet the recording requirements. However, when the study needs to deal with the temperature characteristics, it is still necessary to make a recognition on the temperature characteristic of the capacitance. We found that the time constant of fast capacitance discharge changed with increasing temperature of bath solution when we studied the photothermal effect on cell membrane by patch clamp. Based on this phenomenon, we proposed an equivalent circuit to calculate the temperature-dependent parameters. Experimental results showed that the fast capacitance increased in a positive rate of 0.04 pF/℃, while the pipette resistance decreased. The fine data analysis demonstrated that the temperature rises of bath solution determined the kinetics of the fast capacitance mainly by changing the inner solution resistance of the glass pipette. This result will provide a good reference for the fine temperature characteristic study related to cellular electrophysiology based on patch clamp technique.
Cell Membrane ; Electric Capacitance ; Membrane Potentials ; Patch-Clamp Techniques ; Temperature

OBJECTIVES: Until recently, most patch-clamp recordings in inner hair cells (IHCs) have been performed at room temperature. The results acquired at room temperature should be corrected if they are to be related to in vivo findings. However, the temperature dependency to ion channels in IHCs is unknown. The aim of this study was to investigate the effect of temperature on the potassium currents in IHCs. METHODS: IHCs were isolated from a mature guinea-pig cochlea and potassium currents were recorded at room temperature (around 25degrees C) and physiological temperatures (35degrees C-37degrees C). RESULTS: IHCs showed outwardly rectifying currents in response to depolarizing voltage pulses, with only a slight inward current when hyperpolarized. The amplitude of both outward and inward currents demonstrated no temperature dependency, however, activation and inactivation rates were faster at 36degrees C than at room temperature. Half-time for activation was shorter at 36degrees C than at room temperature at membrane potentials of -10, +10, +20, +30, and +40 mV. Q10 for the activation rate was 1.83. The inactivation time constant in outward tetraethylammonium-sensitive potassium currents was much smaller at 36degrees C than at room temperature between the membrane potentials of -20 and +60 mV. Q10 for the inactivation time constant was 3.19. CONCLUSION: The results of this study suggest that the amplitude of potassium currents in IHCs showed no temperature dependence either in outward or inward-going currents, however, activation and inactivation accelerated at physiological temperatures.
Cochlea ; Dependency (Psychology) ; Hair ; Ion Channels ; Kinetics ; Membrane Potentials ; Potassium

OBJECTIVECurrents contributing repolarization in rabbit ventricular myocyte are very complex since the I(To.s) covers almost the whole repolarization phase of the action potential. The other components of repolarizing currents, as I(Kr) and I(Ks) are small. The purpose of this study is to investigate whether or not there are other currents in rabbit ventricular repolarization.

METHODSIon currents of rabbit ventricular myocyte were recorded using the whole-cell patch-clamp technique.

RESULTSIn the present work, an nonselective cation current was identified by replacing the K(+) with Cs(+) in the bathing and pipette solutions. The outward current elicited by depolarizing potentials could be inhibited by Gd(3+), an effective inhibitor of nonselective cation currents. Depleting Ca(2+) and Mg(2+) in the bathing solution, the amplitudes of this outward current increased by 40%-116% at +60 mV, and adding 2 micromol/L insulin to the solution (with normal concentration of Ca(2+) and Mg(2+) in Tyrode's solution), the amplitude increased by 30%-60% at +60 mV.

CONCLUSIONIt is suggested that a nonselective cation current in rabbit ventricular myocytes may play an important role in the repolarization of the action potential in rabbit ventricle. Changes of nonselective cation current will lead to induce or inhibit arrhythmia.

BACKGROUND: Several different patterns of wavebreak have been described by mapping of the tissue surface during fibrillation. However, it is not clear whether these surface patterns are caused by multiple distinct mechanisms or by a single mechanism. METHODS: To determine the mechanism by which wavebreaks are generated during ventricular fibrillation, we conducted optical mapping studies and single cell transmembrane potential recording in 6 isolated swine right ventricles. RESULTS: Among 763 episodes of wavebreak (0.75 times/sec/cm2), optical maps showed 3 patterns: 80% due to a wavefront encountering the refractory waveback of another wave, 11.5% due to wavefronts passing perpendicularly each other and 8.5% due to a new (target) wave arising just beyond the refractory tail of a previous wave. Computer simulations of scroll waves in 3-D tissue showed that these surface patterns could be attributed to two fundamental mechanisms: head-to-tail interactions and filament break. CONCLUSION: We conclude that during sustained ventricular fibrillation in swine RV, surface patterns of wavebreak are produced by two fundamental mechanisms: head-to-tail interaction between waves and filament break.
Computer Simulation ; Heart Ventricles* ; Membrane Potentials ; Swine* ; Ventricular Fibrillation*

A new denoising method is presented in the paper, based on the independent component analysis(ICA) and the noise independent component selection measurement which is the dispersivity of the independent component's projection coefficients to each electrode. The results indicate that the method can denoise EPM signals with giving prominence to electrodes' true depolarization signals. So it' s fit well for the EPM system.
Electrodes ; Epicardial Mapping ; methods ; Membrane Potentials ; Pericardium ; physiology

Leptin, an adipocyte-derived peptide hormone, has been shown to facilitate breathing. However, the central sites and circuit mechanisms underlying the respiratory effects of leptin remain incompletely understood. The present study aimed to address whether neurons expressing leptin receptor b (LepRb) in the nucleus tractus solitarii (NTS) contribute to respiratory control. Both chemogenetic and optogenetic stimulation of LepRb-expressing NTS (NTS^LepRb) neurons notably activated breathing. Moreover, stimulation of NTS^LepRb neurons projecting to the lateral parabrachial nucleus (LPBN) not only remarkably increased basal ventilation to a level similar to that of the stimulation of all NTS^LepRb neurons, but also activated LPBN neurons projecting to the preBötzinger complex (preBötC). By contrast, ablation of NTS^LepRb neurons projecting to the LPBN notably eliminated the enhanced respiratory effect induced by NTS^LepRb neuron stimulation. In brainstem slices, bath application of leptin rapidly depolarized the membrane potential, increased the spontaneous firing rate, and accelerated the Ca²⁺ transients in most NTS^LepRb neurons. Therefore, leptin potentiates breathing in the NTS most likely via an NTS-LPBN-preBötC circuit.
Leptin/pharmacology* ; Membrane Potentials ; Neurons/metabolism* ; Solitary Nucleus/metabolism*