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PubMed1982

Sympathetic supraspinal control of venous membrane potential in spontaneous hypertension in vivo.

To clarify the mechanisms controlling mesenteric venous membrane potential (Em) in spontaneously hypertensive rats (SHR) and Wistar-Kyoto normotensive rats (WKY), Em was measured in vivo using flexibly mounted glass microelectrodes. Venous diameters were also measured. Ems under control conditions were significantly less in SHR. alpha-Adrenergic blockade with phenoxybenzamine (PBZ) significantly dilated and hyperpolarized SHR small veins but failed to alter the membrane potential of WKY small veins. After blockade with PBZ, membrane potentials were similar in both strains. Propranolol suffusion failed to alter the SHR membrane potential but depolarized WKY small veins. During blockade with PBZ, propranolol depolarized venous membranes equally in both strains. Membrane potentials after spinal section were similar in both strains and equal to the Ems during total adrenergic blockade. The data indicate that, in SHR, the relatively depolarized Em derives from altered alpha-adrenergic input. In SHR, alpha-adrenergic input appears to exert its depolarizing effect, at least in party, by interfering with the expression of endogenous, beta-adrenergic hyperpolarization. The beta-adrenergic influence, like the alpha-adrenergic input in SHR, is dependent on intact supraspinal pathways.

Animals↗
PubMed1991

Determination of the membrane potential of cultured mammalian Schwann cells and its sensitivity to potassium using a thiocarbocyanine fluorescent dye.

The membrane potential of cultured rat sciatic nerve Schwann cells was determined with conventional microelectrode and voltage-sensitive fluorescent dye, Di-S-C3(5), optical techniques. The value for membrane potential obtained with microelectrodes was -42.1 +/- 4.7 mV (n = 8). Using optically determined fluorescent intensity changes caused by changes in external potassium ion concentration, in the presence or absence of valinomycin (null point method), the membrane potential was estimated at -45.7 +/- 6.2 mV (n = 7); with a gramicidin and valinomycin double ionophore method it was -52.2 +/- 9.1 (n = 4). The membrane potential of Schwann cells was found to be potassium sensitive at and above the physiological range of [K+] at 27.5 mV/10x delta[K+], which is approximately half the Nernstian value. This result suggests that other ion permeabilities strongly influence the resting membrane potential of cultured Schwann cells. Since Na+ had little effect on the membrane potential, it is concluded that Cl- is a likely candidate for the other permeant ionic species. The optical method has been shown to be a useful tool for the systematic study of the membrane potential of Schwann cells in culture and for the characterization of its ionic basis and regulation.

Animals↗
PubMed2000

HERG-Like potassium current regulates the resting membrane potential in glomus cells of the rabbit carotid body.

Direct evidence for a specific K(+) channel underlying the resting membrane potential in glomus cells of the carotid body has been absent. The product of the human ether-a-go-go-related gene (HERG) produces inward rectifier currents that are known to contribute to the resting membrane potential in other neuronal cells. The goal of the present study was to determine whether carotid body glomus cells express HERG-like K(+) current, and if so, to determine whether a HERG-like current regulates the resting membrane potential. Freshly dissociated rabbit glomus cells under whole cell voltage clamp exhibited slowly decaying outward currents that activated 20-30 mV positive to the resting membrane potential. Raising extracellular K(+) revealed a slowly deactivating inward tail current indicative of HERG-like K(+) current. HERG-like currents were not found in cells resembling type II cells. The HERG-like current was blocked by dofetilide (DOF) in a concentration-dependent manner (IC(50) = 13 +/- 4 nM, mean +/- SE) and high concentrations of Ba(2+) (1 and 10 mM). The biophysical and pharmacological characteristics of this inward tail current suggest that it is conducted by a HERG-like channel. The steady-state activation properties of the HERG-like current (V(h) = -44 +/- 2 mV) suggest that it is active at the resting membrane potential in glomus cells. In whole cell, current-clamped glomus cells (average resting membrane potential, - 48 +/- 4 mV), DOF, but not tetraethylammonium, caused a significant (13 mV) depolarizing shift in the resting membrane potential. Using fluorescence imaging, DOF increased [Ca(2+)](i) in isolated glomus cells. In an in-vitro carotid body preparation, DOF increased basal sensory discharge in the carotid sinus nerve in a concentration-dependent manner. These results demonstrate that glomus cells express a HERG-like current that is active at, and responsible for controlling the resting membrane potential.

Animals↗
PubMed1997

Spontaneous subthreshold membrane potential fluctuations and action potential variability of rat corticostriatal and striatal neurons in vivo.

We measured the timing of spontaneous membrane potential fluctuations and action potentials of medial and lateral agranular corticostriatal and striatal neurons with the use of in vivo intracellular recordings in urethan-anesthetized rats. All neurons showed spontaneous subthreshold membrane potential shifts from 7 to 32 mV in amplitude, fluctuating between a hyperpolarized down state and depolarized up state. Action potentials arose only during the up state. The membrane potential state transitions showed a weak periodicity with a peak frequency near 1 Hz. The peak of the frequency spectra was broad in all neurons, indicating that the membrane potential fluctuations were not dominated by a single periodic function. At frequencies >1 Hz, the log of magnitude decreased linearly with the log of frequency in all neurons. No serial dependence was found for up and down state durations, or for the time between successive up or down state transitions, showing that the up and down state transitions are not due to superimposition of noisy inputs onto a single frequency. Monte Carlo simulations of stochastic synaptic inputs to a uniform finite cylinder showed that the Fourier spectra obtained for corticostriatal and striatal neurons are inconsistent with a Poisson-like synaptic input, demonstrating that the up state is not due to an increase in the strength of an unpatterned synaptic input. Frequency components arising from state transitions were separated from those arising from the smaller membrane potential fluctuations within each state. A larger proportion of the total signal was represented by the fluctuations within states, especially in the up state, than was predicted by the simulations. The individual state spectra did not correspond to those of random synaptic inputs, but reproduced the spectra of the up and down state transitions. This suggests that the process causing the state transitions and the process responsible for synaptic input may be the same. A high-frequency periodic component in the up states was found in the majority of the corticostriatal cells in the sample. The average size of the component was not different between neurons injected with QX-314 and control neurons. The high-frequency component was not seen in any of our sample of striatal cells. Corticostriatal and striatal neurons' coefficients of variation of interspike intervals ranged from 1.0 to 1.9. When interspike intervals including a down state were subtracted from the calculation, the coefficient of variation ranged from 0.4 to 1.1, indicating that a substantial proportion of spike interval variance was due to the subthreshold membrane potential fluctuations.

Action Potentials↗
PubMed1987

Effect of membrane potential on furosemide-inhibitable sodium influxes in human red blood cells.

Furosemide-inhibitable Na influx (a measure of Na/K/Cl cotransport) was determined as a function of membrane potential in human red blood cells. The membrane potential was varied from -42 to +118 mV using valinomycin and gradients of K. The furosemide-inhibitable, unidirectional Na influx was independent of membrane potential over the entire range of potentials. The change in flux per mV, 0.443 mumol/(liter cells.hr.mV), was not significantly different from zero. The mean flux was 153 +/- 16 mumol/(liter cells.hr) (+/- SEM, n = 71). The ouabain and furosemide-resistant influxes of Na and K were also measured as functions of membrane potential using either valinomycin and K or a chloride-free, tartrate flux medium to vary membrane potential. The unidirectional Na influx decreased slightly as the membrane potential was increased from negative potentials to about +10 mV. At higher membrane potentials Na influx rose dramatically with potential. This increase was not reversible and was also observed with K influx.

Adult↗
PubMed1997

Mitochondrial membrane potential changes in osteoblasts treated with parathyroid hormone and estradiol.

This study assessed mitochondrial membrane potential changes in cultured osteoblasts treated with hormones known to regulate osteoblasts. A fluorescent carbocyanine dye, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine++ + iodide, also called JC-1, was used as a probe. JC-1 emits photons at 585 nm (orange-red) when the membrane potential in mitochondria is highly negative, but when the potential becomes reduced emission occurs at 527 nm (green). Osteoblasts were rinsed in serum-free medium for 5 min, then loaded with 1 x 10(-6) M JC-1 for 10 min. The distribution and intensity of JC-1 fluorescence were evaluated with a laser-scanning confocal microscope system. Hormone treatments included parathyroid hormone (PTH; 10(-8) M), 17beta-estradiol (10(-8) M), and thyroxine (T4; 10(-8) M). The potassium ionophore valinomycin (10(-6) M) was used as a control since it is known to disrupt the electrochemical gradient of mitochondria without interfering with the pH gradient. Valinomycin caused a profound, rapid increase (22.5% above untreated values) in the green/red ratio, which indicated a lowering of the mitochondrial membrane potential in all samples evaluated. PTH caused a less pronounced, but significant (7-14%), reduction in membrane potential in all cells examined. PTH is known to affect osteoblasts in a number of ways and is inhibitory to mitochondrial respiration; the results confirm this effect. For estradiol, half of the cells responded at a significant level, with a membrane potential reduction of 6 to 13% being recorded; the other half did not respond. Thyroxine did not alter mitochondrial membrane potential. Responses were detectable within 20 s for valinomycin, but occurred at a slower rate, over 200 to 300 s, following PTH and estradiol treatment. Responses to PTH and estradiol could be due to mitochondrial uptake of cytosolic Ca2+.

Animals↗
PubMed1981

Inward rectification in frog skeletal muscle fibres and its dependence on membrane potential and external potassium.

1. Experiments were carried out using a voltage-clamp technique to investigate the dependence of inward rectification on membrane potential and on the equilibrium potential for K+, changed either by changing [K]o or changing [K]i. 2. The relationship between gK, the potassium chord conductance, and membrane potential depended on membrane potential and [K]o, but not on [K]i. 3. Under hyperpolarization, K currents increased with time, but instantaneous current-voltage relations also showed inward rectification. The time constants for activation fell with hyperpolarization, e -fold for an 18 mV change in membrane potential. 4. The time constants for activation depended on [K]o but not on [K]i. 5. Under depolarization, the activation of K currents was partly reversed, but between activation and membrane potential, determined from two-pulse experiments, also appeared to depend on [K]o but not on [K]i. 5. Under depolarization, the activation of K currents was partly reversed, but between activation and membrane potential, determined from two-pulse experiments, also appeared to depend on [K]o but not on [K]i. 6. The rate of activation of K currents under hyperpolarization had a Q10 of 2.64 +/- 0.08 (n = 5). Currents, measured per unit length, increased with temperature, with a Q10 of 1.66 +/- 0.11 (n = 5).

Animals↗
PubMed1968

Membrane potential of brown adipose tissue. A suggested mechanism for the regulation of thermogenesis.

Membrane potentials were recorded in isolated segments of interscapular brown adipose tissue from rats. After equilibration at 29 degrees C in Krebs-Ringer bicarbonate buffer a mean value of -51 +/- 4 mv (SD) was found. This level could be maintained for up to 5 hr. The mean effective membrane resistance was 1.35 +/- 0.45 megohm. The membrane potential was a function of the extracellular potassium concentration. Ouabain (10(-6)-10(-3)M) and incubation in K-free buffer produced progressive depolarization. Epinephrine and norepinephrine in concentrations as low as 10(-8) g/ml produced a prompt depolarization. Cooling of the tissue and lowering of the oxygen tension caused a marked and reversible decrease in the membrane potential. In tissue obtained from cold-adapted rats, the membrane potential was considerably diminished. 6Assuming that the membrane potential is some function of the Na permeability of the plasma membrane it is suggested that an increase in the rate of active Na-K transport and ensuing ADP formation might contribute to the increase in respiration seen during exposure to thermogenic stimuli.

Adaptation, Physiological↗
PubMed1980

Control of membrane potential by external H+ concentration in Bacillus subtilis as determined by an ion-selective electrode.

The membrane potential of intact bacteria was monitored by measuring the tetraphenylphosphonium ion distribution across the membrane using poly--(vinyl chloride) matrix-type electrode selective to tetraphenylphosphonimum ion. It was found that the tetraphenylphosphonium ion was not countertransported against H+ movement. The membrane potential of Bacillus subtilis was estimated to be 80-120 mV inside-negative at external pH 7. The effect of the external pH on the membrane potential was studied. It varied from 30 to 40 mV/decade change in the external [H+] in the pH region of greater than 6.5, increasing pH making it more inside-negative. The addition of carbonyl cyanide m-chlorophenylhydrazone depolarized the membrane, and the membrane potential approached the H+ equilibrium potential. The addition of N,N'-dicyclohexylcarbodiimide did not abolish the pH dependence of the membrane potential. Increasing the external [K+] did not affect the pH dependence. CN- partially depolarized the membrane. A parallel conductance model for membrane potential could explain the results qualitatively.

Bacillus subtilis↗
PubMed1985

Cyanine dye fluorescence used to measure membrane potential changes due to the assembly of complement proteins C5b-9.

The fluorescent potentiometric indicator diS-C3-(5) has been used to investigate changes in membrane potential due to assembly of the C5b-9 membrane attack complex of the complement system. EAC1-7 human red blood cells and resealed erythrocyte ghosts--bearing membrane-assembled C5b67 complexes--were generated by immune activation in C8-deficient human serum. Studies performed with these cellular intermediates revealed that the membrane potential of EAC1-7 red cells and ghosts is unchanged from control red cells (-7 mV) and ghosts (O mV), respectively. Addition of complement proteins C8 and C9 to EAC1-7 red cells results in a dose-dependent depolarization of membrane potential which precedes hemolysis. This prelytic depolarization of membrane potential--and the consequent onset of hemolysis--is accelerated by raising external [K+], suggesting that the diffusional equilibration of transmembrane cation gradients is rate limiting to the cytolytic event. In the case of EAC1-7 resealed ghosts suspended at either high external [K+] or [Na+], no change in membrane potential (from O mV) could be detected after C8/C9 additions. When the membrane potential of the EAC1-7 ghost was displaced from O mV by selectively increasing the K+ conductance with valinomycin, a dose-dependent depolarization of the membrane was observed upon addition of C8 and C9. In these experiments, lytic breakdown of the ghost membranes was less than 5%. Conclusions derived from this study include: (i) measured prelytic depolarization of the red cell Donnan potential directly confirms the colloid-osmotic theory of immune cytolysis. (ii) The diffusional transmembrane equilibration of Na+ and K+ through the C5b-9 pore results in a dose-dependent depolarization of the membrane potential (Em) which appears to be rate-limiting to cytolytic rupture of the target erythrocyte. (iii) Enhanced immune hemolysis observed in high K+ media cannot be attributed to cation-selective conductance across the C5b-9 pore, and is probably related to the near-equilibrium condition of potassium-containing red cells when suspended at high external K+. These experiments demonstrate that carbocyanine dye fluorescent indicators can be used to monitor electrochemical changes arising from immune damage to the plasma membrane under both cytolytic and noncytolytic conditions. Potential application of this method to the detection of sublytic pathophysiological changes in the plasma membrane of complement-damaged cells are discussed.

Complement Membrane Attack Complex↗
PubMed1987

Membrane potential of stored platelets and its effect on platelet functions.

Relationships among intracellular Ca2+ level, membrane potential in resting state and platelet functions were examined. Membrane potential of platelets was increased (hyperpolarized) during storage and decreased (depolarized) by 37 degrees C incubation with plasma after storage. The degree of depolarization was greater in fresh plasma than in stored plasma. Changes of platelet functions were reverse with the membrane potential change. Aggregation induced by ADP or collagen was enhanced by depolarization with increasing extracellular [K+]. Shrinkage ratio (hypotonic shock response) of stored platelet which were hyperpolarizing, exhibited optimal value when the membrane potential was slightly depolarized. Intracellular [Ca2+] was not affected by the extracellular [K+]. These results suggest that platelet sensitivity is controlled by the membrane potential in resting state.

Blood Platelets↗
PubMed1993

Fluctuations in pyramid-pyramid excitatory postsynaptic potentials modified by presynaptic firing pattern and postsynaptic membrane potential using paired intracellular recordings in rat neocortex.

Single axon excitatory connections between pairs of neocortical pyramidal neurons were studied using paired intracellular recordings in layers II/III and IV of coronal slices of adult rat somatosensory/motor cortex. Excitatory postsynaptic potentials evoked with different presynaptic firing patterns and at different postsynaptic membrane potentials were compared. Two methods of statistical analysis were used in attempts to determine whether changes in mean excitatory postsynaptic potential amplitude were due to presynaptic or postsynaptic modifications. Analysis of the decrease in mean excitatory postsynaptic potential amplitude associated with increases in presynaptic firing rate were consistent with a change in probability of transmitter release. Paired pulse depression appeared to exhibit both presynaptic and postsynaptic components when the interspike interval was < 10 ms, but could be explained simply by a decrease in probability of release with interspike intervals between 10 and 80 ms. Previous studies had demonstrated that these excitatory postsynaptic potentials are partially mediated by N-methyl-D-aspartate receptors. In contrast to the apparently presynaptic effects of firing pattern, postsynaptic membrane depolarization appeared to produce an increase in quantal amplitude. In addition to this increase at low frequencies, a form of frequency-dependent, self-potentiation involving the recruitment of an additional, longer-latency postsynaptic component occurred at higher presynaptic firing rates. The possibility is discussed that two different mechanisms are involved in the replacement of vesicles at release sites. Over a few tens of milliseconds (paired-pulse depression) availability of releasable transmitter may be determined by the rate of replacement of discharged vesicles from a readily releasable pool of vesicles. Over longer periods of firing at 0.33-2 Hz, the readily releasable pool may become exhausted and require replenishment. Postsynaptic depolarization increases the duration of these excitatory postsynaptic potentials, facilitating summation and enables two components of excitatory postsynaptic potential enhancement at N-methyl-D-aspartate receptor-mediated synapses; one that is present at all firing rates and relates simply to voltage dependent events and one that occurs at higher firing rates and involves a gradual, time dependent event. These data also indicate that the optimal pyramidal firing pattern if another pyramid is to be activated is a tonic, or brief burst pattern at relatively low repetition rates. Long bursts of many presynaptic spikes recruit little that is not activated by pairs of spikes. This situation is in stark contrast to the results obtained in the following paper in which excitatory inputs from pyramids to non-pyramids are described.

Animals↗
PubMed2002

Disruption of the two-state membrane potential of striatal neurones during cortical desynchronisation in anaesthetised rats.

In anaesthetised animals, the very negative resting membrane potential of striatal spiny neurones (down state) is interrupted periodically by depolarising plateaux (up states) which are probably driven by excitatory input. In the absence of active synaptic input, as occurs in vitro, potassium currents hold the membrane potential of striatal spiny neurones in the down state. Because striatal spiny neurones fire action potentials only during the up state, these plateau depolarisations have been perceived as enabling events that allow information processing through cerebral cortex-basal ganglia circuits. Recent studies have demonstrated that the robust membrane potential fluctuation of spiny neurones is strongly correlated to the slow electroencephalographic rhythms that are typical of slow wave sleep and anaesthesia. To further understand the impact of cortical activity states on striatal function, we studied the membrane potential of striatal neurones during cortical desynchronised states. Simultaneous in vivo recordings of striatal neurones and the electrocorticogram in urethane-anaesthetised rats revealed that rhythmic alternation between up and down states was disrupted during episodes of spontaneous or induced cortical desynchronisation. Instead of showing robust two-state fluctuations, the membrane potential of striatal neurones displayed a persisting depolarised state with fast, low-amplitude modulations. Spiny neurones remained in this persistent up state until the cortex resumed ~1 Hz synchronous activity. Most of the recorded neurones exhibited a low firing probability, irrespective of the cortical activity state. Time series analysis failed to reveal significant correlations between the membrane potential of striatal neurones and the desynchronised electrocorticogram. Our results suggest that during cortical desynchronisation continuous uncorrelated excitatory input sustains the membrane potential of striatal neurones in a persisting depolarised state, but that substantial additional input is necessary to impel the neurones to threshold. Our data support that the prevailing cortical activity state determines the duration of the enabling depolarising events that take place in striatal spiny neurones.

Anesthesia↗
PubMed1998

Carbachol-induced oscillations in membrane potential and [Ca2+]i in guinea-pig ileal smooth muscle cells.

1. Cytosolic free Ca2+ concentration ([Ca2+]i) and membrane potential were simultaneously recorded from single smooth muscle cells of guinea-pig ileum, using a combination of nystatin-perforated patch clamp and fura-2 fluorimetry techniques. 2. Carbachol (CCh, 2 microM) produced oscillatory changes in [Ca2+]i and membrane potential which coincided well in time with each other, and peaks of membrane potential oscillations reached a saturated level of around -7 mV. Thapsigargin (1 microM) abolished these effects of 2 microM CCh. La3+ (3 microM) immediately prevented the discharge of spike potentials, but allowed both on-going oscillatory responses to persist for a while. 3. CCh (0.25-0.75 microM) caused membrane potential and [Ca2+]i to oscillate in some 20 % of cells studied. Every membrane potential oscillation was preceded by the discharge of single or multiple spike potentials. The effects of CCh were readily abolished by La3+ (3 microM). 4. In cells exhibiting no oscillatory response to 0.25-0.75 microM CCh, an electrically evoked action potential usually generated changes in [Ca2+]i and membrane potential similar to those following spontaneously evoked action potentials, and sometimes it did so only after [Ca2+]i or InsP3 had been slightly elevated by repeatedly evoking action potentials or by increasing CCh concentration in the bath medium. 5. The results suggest that in ileal smooth muscle cells, the oscillations of [Ca2+]i and membrane potential arising from muscarinic stimulation result from release of Ca2+ from internal stores and that there is a Ca2+-induced potentiation of coincidently elicited cation channel openings. Under weak muscarinic stimulation, Ca2+ entry upon action potential discharge can trigger such a release of stored Ca2+, resulting in synchronous generation of a large rise in [Ca2+]i and a slow, large membrane depolarization.

Action Potentials↗
PubMed1987

Ionic dependence of membrane potential and glutamate receptor-linked responses in synaptoneurosomes as measured with a cyanine dye, DiS-C2-(5).

Membrane potentials of particles present in a subcellular brain preparation, called synaptoneurosomes, have been monitored by measurement of changes in the absorbance of a cyanine dye, DiS-C2-5. The membrane potential of the particles seems to be dependent on both Cl- and K+ diffusion potentials, as judged from dependence of the absorbance changes on the K+ equilibrium potential across the membrane in the presence of Ba2+ or when Cl- was replaced with gluconate. The apparent high Cl- permeability of the membrane preparation was reduced in the presence of picrotoxin, a finding suggesting endogenous activation of receptor-linked Cl- channels. Glutamate and kainate caused depolarization of the membranes present in the preparation. This effect was only seen if K+ channels had been blocked in the presence of Ba2+ or 4-aminopyridine. No responses were observed with other glutamate receptor agonists (quisqualate or N-methyl-D-aspartate). The membrane potential of particles present in conventional synaptosomal preparations neither had a high Cl- permeability nor reacted to glutamate or kainate in the present conditions. The results suggest that synaptoneurosome preparations may be used for functional studies on postsynaptic neurotransmitter receptor-linked membrane potential changes with optical probes of membrane potential.

Animals↗
PubMed1982

Alternative methods for measurement of membrane potentials in epithelia.

Methods for the measurement of membrane potentials in cells not easily penetrated by microelectrodes were assessed for use in epithelia. The lipophilic cation triphenylmethylphosphonium appeared to distribute in a Nernstian fashion in the epithelial cells of Necturus gallbladder as judged by parallel microelectrode measurements. In the toad urinary bladder, the distribution of this cation gave a value for the membrane potential of epithelial cells under short-circuit conditions of -62 mV in normal Ringer's solution and -51 mV after 2 h treatment with ouabain. In our laboratory the dye 3,3'-dipropylthiadicarbocyanine iodide, when used with cell suspensions, yielded results comparable to those of other workers, but we were unable to record a redistributional signal from epithelial sheets or scraped cells. The dye appeared to enter cells and become irreversibly bound. The membrane-bound merocyanine dyes have not been used on epithelial cells. They appear to hold the greatest promise for dynamic experiments on epithelial membrane potentials.

Animals↗
PubMed1993

[Effect of sevoflurane on contraction and membrane potentials in canine right ventricular myocytes].

The effects of sevoflurane on contraction and membrane potentials were studied in isolated canine ventricular muscle strips. Sevoflurane depressed electrically-induced contraction in a dose-dependent manner. The inhibitory effect was more pronounced in high-K+ Tyrode solution than in normal Tyrode solution suggesting that sevoflurane inhibits transmembrane Ca2+ influx. In electrophysiological studies, sevoflurane depressed both overshoot and the plateau phase of action potentials. Resting membrane potential was not affected by sevoflurane. We conclude that the depression of myocardial contractility by sevoflurane may be due to block of transmembrane calcium influx.

Action Potentials↗