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PubMed1982

The use of fluorescent dyes to measure membrane potentials: a response.

The use of fluorescent cyanine dyes to estimate membrane potential in cell suspensions has been considered. Several problems related tot he application of the dyes have been reviewed. These problems include: 1) alteration of the membrane potential (Em) and factors involved in establishing Em by the dyes themselves, 2) the effects of altered energy metabolism on the fluorescent response of the dyes and on Em, and 3) calibration of dye fluorescence. Recent reports that advocate the use of the fluorescent dyes are misleading.

Adenosine Triphosphate↗
PubMed2006

Oscillatory membrane potential response to glucose in islet beta-cells: a comparison of islet-cell electrical activity in mouse and rat.

In contrast to mouse, rat islet beta-cell membrane potential is reported not to oscillate in response to elevated glucose despite demonstrated oscillations in calcium and insulin secretion. We aim to clarify the electrical activity of rat islet beta-cells and characterize and compare the electrical activity of both alpha- and beta-cells in rat and mouse islets. We recorded electrical activity from alpha- and beta-cells within intact islets from both mouse and rat using the perforated whole-cell patch clamp technique. Fifty-six percent of both mouse and rat beta-cells exhibited an oscillatory response to 11.1 mm glucose. Responses to both 11.1 mm and 2.8 mm glucose were identical in the two species. Rat beta-cells exhibited incremental depolarization in a glucose concentration-dependent manner. We also demonstrated electrical activity in human islets recorded under the same conditions. In both mouse and rat alpha-cells 11 mm glucose caused hyperpolarization of the membrane potential, whereas 2.8 mm glucose produced action potential firing. No species differences were observed in the response of alpha-cells to glucose. This paper is the first to demonstrate and characterize oscillatory membrane potential fluctuations in the presence of elevated glucose in rat islet beta-cells in comparison with mouse. The findings promote the use of rat islets in future electrophysiological studies, enabling consistency between electrophysiological and insulin secretion studies. An inverse response of alpha-cell membrane potential to glucose furthers our understanding of the mechanisms underlying glucose sensitive glucagon secretion.

Animals↗
PubMed1995

Changes in amino acid release and membrane potential during cerebral hypoxia and glucose deprivation.

Excessive release of glutamate is believed to play a major role in the susceptibility of neurons to ischaemia. Whether the glutamate release is the primary event or occurs in response to electrophysiologic alterations has not been clarified. In the present study, the amino acid release was therefore correlated to changes in electrophysiological parameters and energy status during conditions of low oxygen tension and varying glucose concentrations in rat hippocampal slices. Plain hypoxia failed to produce glutamate release. All neurons underwent, however, a slow depolarization causing most of the neurons to lose their membrane potential within 10 minutes. By restoring the membrane potential to resting level by current injection, the neurons could still be activated synaptically and respond to transmitter application. Following reoxygenation most of the cells regained their resting membrane potential, but showed reduced excitability. When the slices were exposed to hypoxia combined with glucose deprivation (simulated ischaemia), there was a pronounced increase in the glutamate release. This glutamate release was always preceded by a fast anoxic depolarization. Whereas hypoxia reduced the ATP content only to approximately 50%, ATP was depleted in slices exposed to simulated ischaemia. The results demonstrate that although the neurons lose their membrane potential completely during hypoxia, there is no glutamate release. A fast anoxic depolarization provoked by simulated ischaemia, however, is always followed by glutamate release, probably due to a more severe ATP depletion.

Amino Acids↗
PubMed1988

Intracellular pH influences the resting membrane potential of isolated rat hepatocytes.

This study in isolated rat hepatocytes sought to determine if the changes in membrane potential associated with intracellular alkalinization or acidification could be attributed to changes in K+ conductance. Intracellular pHi was manipulated using the 'NH4+-pulse' method: inducing intracellular alkalinization with NH4Cl (10 mM), and producing acidification by diluting the NH4+-loaded cells with ammonium ion-free buffer or by adding sodium proprionate. Membrane potential and resistance were measured in freshly isolated rat liver cells using intracellular microelectrodes. The results indicated that intracellular alkalinization was associated with hyperpolarization and decreased membrane resistance, whereas intracellular acidification caused depolarization with increased membrane resistance. As pHi-mediated electrogenic responses have been related to changes in K+ conductance in other epithelial tissues, the influence of K+ transport inhibitors on NH4+-evoked electrical effects was examined. NH4Cl-evoked membrane potential changes were inhibited by the K+ channel blockers, quinine and barium and in potassium depolarized cells (cells bathed in a high K+ medium where [K+]in = [K+]out = 140 mM). Furthermore, Rubidium-86 (86Rb+) efflux from preloaded hepatocytes, a measure of K+ permeability, was enhanced following intracellular alkalinization but inhibited by intracellular acidification. Thus, these results indicate that pHi-evoked electrogenic effects in hepatocytes are mediated through changes in K+ conductance.

Ammonium Chloride↗
PubMed1971

Membrane potentials and ion permeability in a cation exchange membrane.

The nonequilibrium electrical potentials across an artificial membrane bathed by solutions of a single salt have been measured and calculated using the Goldman-Hodgkin-Katz equation and the irreversible thermodynamic equation. The latter equation predicts the observed potential differences over a 2500-fold concentration range, while application of a modified Goldman-Hodgkin-Katz equation leads to difficulties.

Biological Transport↗
PubMed2001

Rat Coronary Endothelial Cell Membrane Potential Responses During Hypertension.

-The purpose of this study was to provide the first membrane potential profile in coronary endothelial cells from normotensive sham-operated control and 1-kidney, 1-clip renal hypertensive rats. Dilator responses were assessed in cannulated coronary arteries from control and 1-kidney, 1-clip rats, and the perforated patch-clamp method was used to compare membrane potential responses between the intact endothelial cells. Under these conditions, acetylcholine (100 pmol/L to 10 µmol/L) induced similar large dilations of coronary arteries from control and 1-kidney, 1-clip rats that were associated with endothelial cell hyperpolarizing responses of 16+/-3 and 18+/-2 mV, respectively. Substance P (10 fmol/L to 1 nmol/L) and bradykinin (100 fmol/L to 10 nmol/L) also substantially dilated coronary arteries from control rats but only induced small (2 to 4 mV) endothelial cell hyperpolarizing responses. These dilations, which appeared independent of membrane potential changes, were highly blunted or absent in arteries from 1-kidney, 1-clip rats. Thus, dilator responses to acetylcholine that are associated with large endothelial hyperpolarizing responses are normal in the small coronary arteries of 1-kidney, 1-clip rats. However, dilator response to substance P and bradykinin, which apparently are not heavily dependent on endothelial cell hyperpolarizations, are selectively targeted for impairment in the coronary arteries of this model of hypertension

Journal Article↗
PubMed1979

Cation transport and membrane potential properties of primary astroglial cultures from neonatal rat brains.

This paper describes K+ and Na+ content and transport in primary monolayer cultures from dissociated newborn rat brains, considered to consist predominantly of astroglial cells. Net changes in cation content after addition of ouabain, and steady state fluxes using 86Rb+ as a marker for K+ and 22Na+ as a marker for Na+, were measured. The results found indicate that the cells maintained a conventional pattern of cation homeostasis with net efflux of K+ being balanced by its active uptake and net uptake of Na+ balanced by active extrusion mediated by a ouabain sensitive (Na+K) pump. These processes maintained internal measured K+:Na+ ratios of 12--25:1. The cells were normally flat but addition of DBcAMP caused them to round up and form numerous processes, an appearance resembling that of astroglial cells in vivo. DBcAMP treatment also reduced the steady state levels of K+ measured with 86Rb+ by 15--30%, and had no effect on initial rates of 86Rb+ and 22Na+ uptake. The membrane potentials of cells treated with DBcAMP were studied, since only these were easily impaled. The membrane potentials of separate groups of cells gave means ranging from --65 to --75 mV at 35 degrees C, at an external K+ concentration ([K+]o) of 4.5 mM. The dependence of the membrane potentials of individual cells and groups of cells on [K+]o was studied. The slope of the potential per 10-fold change in [K+]o was 55--57 mV, at concentrations of K+ greater than 10--20 mM K+, and diverged from this slope at concentrations below this. This shows that these cells had some permeability to ions other than K+. Assuming that Na+ was the only other ion affecting the membrane potential, it was calculated that the permeability to Na+ was about 30 times less than K+. A similar result was obtained based on estimates of Na+ and K+ permeability from transport experiments on cells also treated with DBcAMP. The results obtained from these cells are compared to those found for other cultured glial cells and glial cells in vivo. We conclude that the membrane potentials of the cultured cells used in the present study show the closest resemblance so far to glia in vivo, since they are large and negative and are determined mainly by K+. However, the cultured cells have different properties from those reported in some studies for glial cells in vivo by showing free permeability to ions other than K+.

Animals↗
PubMed1996

Yeast mitochondria lacking the phosphate carrier/p32 are blocked in phosphate transport but can import preproteins after regeneration of a membrane potential.

Two different functions have been proposed for the phosphate carrier protein/p32 of Saccharomyces cerevisiae mitochondria: transport of phosphate and requirement for import of precursor proteins into mitochondria. We characterized a yeast mutant lacking the gene for the phosphate carrier/p32 and found both a block in the import of phosphate and a strong reduction in the import of preproteins transported to the mitochondrial inner membrane and matrix. Binding of preproteins to the surface of mutant mitochondria and import of outer membrane proteins were not inhibited, indicating that the inhibition of protein import occurred after the recognition step at the outer membrane. The membrane potential across the inner membrane of the mutant mitochondria was strongly reduced. Restoration of the membrane potential restored preprotein import but did not affect the block of phosphate transport of the mutant mitochondria. We conclude that the inhibition of protein import into mitochondria lacking the phosphate carrier/p32 is indirectly caused by a reduction of the mitochondrial membrane potential (delta(gamma)), and we propose a model that the reduction of delta(psi) is due to the defective phosphate import, suggesting that phosphate transport is the primary function of the phosphate carrier/p32.

Adenosine Triphosphate↗
PubMed1985

The effects of ionophore A23187 and concanavalin A on the membrane potential of human peripheral blood lymphocytes and rat thymocytes.

Effects of the Ca2+-ionophore A23187 and concanavalin A on the membrane potential of human lymphocytes and rat thymocytes have been studied using the fluorescent potential probe diS-C3-(5). At concentrations of 10(-8) to 10(-6) M A23187 changes the membrane potential, inducing both hyper- and depolarization. Depending on concentrations of A23187 and the external Ca2+, and on the type of lymphocytes, one of these effects predominates. The hyperpolarization induced by A23187 is caused by activation of Ca2+-dependent K+ channels. It is blocked by quinine and high concentrations of extracellular K+. The dependence of Ca2+-activated K+ transport on extracellular Ca2+ and its sensitivity to calmodulin antagonists is different for human lymphocytes and for thymocytes. As distinct from lymphocytes, in thymocytes calmodulin is not involved in activation of Ca2+-dependent K+ transport. The depolarization induced in lymphocytes by A23187 is caused by an increase in Na+ permeability of the lymphocyte plasma membrane: it is eliminated in a low-Na+ medium. At mitogenic concentrations concanavalin A does not change the membrane potential of the lymphocytes. The results obtained permit elucidation of the relationship between two early events in lymphocyte activation, namely the increase in intracellular Ca2+ concentration and the increase in lymphocyte plasma membrane permeabilities to monovalent cations.

Animals↗
PubMed2000

Spinal nerve injury enhances subthreshold membrane potential oscillations in DRG neurons: relation to neuropathic pain.

Primary sensory neurons with myelinated axons were examined in vitro in excised whole lumbar dorsal root ganglia (DRGs) taken from adult rats up to 9 days after tight ligation and transection of the L(5) spinal nerve (Chung model of neuropathic pain). Properties of subthreshold membrane potential oscillations, and of repetitive spike discharge, were examined. About 5% of the DRG neurons sampled in control DRGs exhibited high-frequency, subthreshold sinusoidal oscillations in their membrane potential at rest (V(r)), and an additional 4.4% developed such oscillations on depolarization. Virtually all had noninflected action potentials (A(0) neurons). Amplitude and frequency of subthreshold oscillations were voltage sensitive. A(0) neurons with oscillations at V(r) appear to constitute a population distinct from A(0) neurons that oscillate only on depolarization. Axotomy triggered a significant increase in the proportion of neurons exhibiting subthreshold oscillations both at V(r) and on depolarization. This change occurred within a narrow time window 16-24 h postoperative. Axotomy also shifted the membrane potential at which oscillation amplitude was maximal to more negative (hyperpolarized) values, and lowered oscillation frequency at any given membrane potential. Most neurons that had oscillations at V(r), or that developed them on depolarization, began to fire repetitively when further depolarized. Spikes were triggered by the depolarizing phase of oscillatory sinusoids. Neurons that did not develop subthreshold oscillations never discharged repetitively and rarely fired more than a single spike or a short burst, on step depolarization. The most prominent spike waveform parameters distinguishing neurons capable of generating subthreshold oscillations, and hence repetitive firing, was their brief postspike afterhyperpolarization (AHP) and their low single-spike threshold. Neurons that oscillated at V(r) tended to have a more prolonged spike, with slower rise- and fall-time kinetics, and lower spike threshold, than cells that oscillated only on depolarization. The main effects of axotomy were to increase spike duration, slow rise- and fall-time kinetics, and reduce single-spike threshold. Tactile allodynia following spinal nerve injury is thought to result from central amplification ("central sensitization") of afferent signals entering the spinal cord from residual intact afferents. The central sensitization, in turn, is thought to be triggered and maintained in the Chung model by ectopic firing originating in the axotomized afferent neurons. Axotomy by spinal nerve injury enhances subthreshold membrane potential oscillations in DRG neurons, augments ectopic discharge, and hence precipitates neuropathic pain.

Action Potentials↗
PubMed1980

The effect of gamma-aminobutyric acid on the input conductance and membrane potential of Ascaris muscle.

1 Twin intracellular recordings were made from the bag region of Ascaris muscle in order to make conductance measurements. The preparation was bathed in a cool (22 degrees C) Ringer solution to abolish the large spontaneous depolarizing potentials and to improve stability for recording.2 The resting membrane potential was -31 +/- 1 mV, mean +/- s.e. mean (n = 17). The current-voltage plots were linear in the hyperpolarizing direction but showed evidence of delayed rectification during the application of depolarizing currents. The input conductance of the bag was measured from the slope of these plots during the application of hyperpolarizing current. The resting conductance of the bags was 2.4 +/- 0.2 muS, mean +/- s.e. mean (n = 12).3 When the preparation was perfused with gamma-aminobutyric acid (GABA) in concentrations greater than 3 muM, a dose-dependent increase in conductance associated with a hyperpolarizing potential was recorded. The log dose-response relationship obtained from 6 preparations was sigmoidal and had an ED(50) of 13 muM.4 When Cl(-) in the Ringer was replaced by SO(4) (2-), the GABA-induced conductance changes decreased and were associated with depolarizing potentials.5 Voltage responses were recorded in the bag region during the iontophoretic application of GABA to different regions of the muscle cell. The largest responses were recorded when GABA was applied to the bag region. Smaller responses were recorded when GABA was applied to the arms and syncytial regions. The responses of the bags were dose-dependent and were antagonized by bath-applied picrotoxin.6 An extrapolation method using 10(-5) M GABA suggested that the GABA reversal potential was about 30 mV more negative than the resting membrane potential. This was confirmed by means of a two microelectrode voltage clamp technique. The reversal potential was thus estimated as -61.2 +/- 2.2 mV mean +/- s.e. mean (n = 27).

Animals↗
PubMed1996

Modulation of cell membrane potential in cultured vascular endothelium.

The present study explores the role of different ionic conductances in the regulation of membrane potential under resting conditions and after bradykinin (BK) or thapsigargin (TG) stimulation of cultured bovine aortic endothelial cells. Under resting conditions, the cell membrane potential observed was -62+/- 5 mV. The main conductance under these conditions is an inwardly rectifying potassium (IRK) channel. Application of 50 nM BK induced a transient hyperpolarization to -87 +/- 4 mV followed by sustained depolarization to -35 +/- 5 mV. The transient hyperpolarization was eliminated by 1 microM noxiustoxin, a blocker of calcium-activated postassium channels (K(Ca)). the sustained depolarization induced by BK was prevented by incubating the cells with the calcium channel blocker lanthanum. TG evoked a similar response in membrane potential, with the exception that the onset of the hyperpolarization was slower compared with BK. The results presented here indicate that the cell resting potential is maintained at -62 +/- 2 mV by the IRK channel. BK or TG stimulation induces a transient hyperpolarization of approximately -20 mV produced by activation of a KCa. This hyperpolarization is followed by a sustained depolarization produced by activation of a calcium-selective channel sensitive to lanthanum.

Animals↗
PubMed2003

Resting membrane potential regulates Na(+)-Ca2+ exchange-mediated Ca2+ overload during hypoxia-reoxygenation in rat ventricular myocytes.

In the heart, reperfusion following an ischaemic episode can result in a marked increase in [Ca2+]i and cause myocyte dysfunction and death. Although the Na(+)-Ca2+ exchanger has been implicated in this response, the ionic mechanisms that are responsible have not been identified. In this study, the hypothesis that the diastolic membrane potential can influence Na(+)-Ca2+ exchange and Ca2+ homeostasis during chemically induced hypoxia-reoxygenation has been tested using right ventricular myocytes isolated from adult rat hearts. Superfusion with selected [K+]o of 0.5, 2.5, 5, 7, 10 and 15 mM yielded the following resting membrane potentials: -27.6+/-1.63 mV, -102.2+/-1.89, -86.5+/-1.03, -80.1+/-1.25, -73.6+/-1.02 and -66.4+/-1.03, respectively. In a second set of experiments myocytes were subjected to chemically induced hypoxia-reoxygenation at these different [K+]o, while [Ca2+]i was monitored using fura-2. These results demonstrated that after chemically induced hypoxia-reoxygenation had caused a marked increase in [Ca2+]i, hyperpolarization of myocytes with 2.5 mM [K+]o significantly reduced [Ca2+]i (7.5+/-0.32 vs. 16.9+/-0.55%); while depolarization (with either 0.5 or 15 mM [K+]o) significantly increased [Ca2+]i (31.8+/-3.21 and 20.8+/-0.36 vs. 16.9+/-0.55%, respectively). As expected, at depolarized membrane potentials myocyte hypercontracture and death increased in parallel with Ca2+ overload. The involvement of the Na(+)-Ca2+ exchanger in Ca2+ homeostasis was evaluated using the Na(+)-Ca2+ exchanger inhibitor KB-R7943. During reoxygenation KB-R7943 (5 microM) almost completely prevented the increase in [Ca2+]i both in control conditions (in 5 mM [K+]o: 2.2+/-0.40 vs. 10.8+/-0.14%) and in depolarized myocytes (in 15 mM [K+]o: -2.1+/-0.51 vs. 11.3+/-0.05%). These findings demonstrate that the resting membrane potential of ventricular myocytes is a critical determinant of [Ca2+]i during hypoxia-reoxygenation. This appears to be due mainly to an effect of diastolic membrane potential on the Na(+)-Ca2+ exchanger, since at depolarized potentials this exchanger mechanism operates in the reverse mode, causing a significant Ca2+ influx.

Animals↗
PubMed2005

Feedback effects of horizontal cell membrane potential on cone calcium currents studied with simultaneous recordings.

Horizontal cell (HC) to cone feedback helps establish the center-surround arrangement of visual receptive fields. It has been shown that HC activity influences cone synaptic output by altering the amplitude and voltage dependence of the calcium current (ICa) in cones. In this study, we obtained voltage-clamp recordings simultaneously from cones and HCs to directly control the membrane potential of HCs and thereby measure the influence of HC membrane potential changes on ICa in adjacent cones. Directly hyperpolarizing voltage clamped HCs produced a negative activation shift and increased the amplitude of ICa in cones. Both of these effects were abolished by enhancing extracellular pH buffering capacity with HEPES. In contrast, addition of the gap junction blocker, carbenoxolone, did not significantly alter the shifts or amplitude changes in cone ICa produced by changes in HC membrane potential. These results support the hypothesis that changes in the HC membrane potential alter the voltage dependence and amplitude of cone ICa by altering extracellular pH levels at the synapse.

Animals↗
PubMed1982

Measurement of membrane potential in polymorphonuclear leukocytes and its changes during surface stimulation.

The membrane potential of guinea pig polymorphonuclear leukocytes has been assessed with two indirect probes, tetraphenylphosphonium (TPP+) and 3,3'-dipropylthiadicarbocyanine (disS-C3-(5)). The change in TPP+ concentration in the medium was measured with a TPP+-selective electrode. By monitoring differences in accumulation of TPP+ in media containing low and high potassium concentrations, a resting potential of -58.3 mV was calculated. This potential is composed of a diffusion potential due to the gradient of potassium, established by the Na+, K+ pump, and an electrogenic potential. The chemotactic peptide fMet-Leu-Phe elicits a rapid efflux of accumulated TPP+ (indicative of depolarization) followed by its reaccumulation (indicative of repolarization). In contrast, stimulation with concanavalin A results in a rapid and sustained depolarization without a subsequent repolarization. The results obtained with TPP+ and diS-C3-(5) were comparable. Such changes in membrane potential were observed in the absence of extracellular sodium, indicating that an inward movement of sodium is not responsible for the depolarization. Increasing potassium levels, which lead to membrane depolarization, had no effect on the oxidative metabolism in nonstimulated or in fMet-Leu-Phe-stimulated cells. Therefore, it seems unlikely that membrane depolarization per se is the immediate stimulus for the respiratory burst.

Animals↗
PubMed1984

Effect of veratridine on membrane potential of sartorius muscle from Rana pipiens.

The effect of veratridine on the membrane potential of sartorius muscles from Rana pipiens was studied. Membrane potential (Vm) was measured in Ringer solutions containing 2.5, 10, 30, 75, and 190 mM K+ in the absence and presence of veratridine. The product [K]o[Cl]o was kept at 300 mM2 to maintain Donnan equilibrium. External Na+ was lowered to 10 mM. Ouabain (100 microM) was present in all solutions. Vm vs. log [K]o curves were fit using the Goldman-Hodgkin-Katz equation with a single free parameter, alpha = PNa/PK (permeability ratio of Na to K). Veratridine (100 microM) causes alpha to increase 12.6 +/- 1.2-fold (n = 9), from 0.146 to 1.657. The effect of veratridine on Vm is dose dependent and reversible, with a time constant for washout of 40 min. The depolarization produced by veratridine is prevented by tetrodotoxin and by Mg, is sensitive to external Na concentration, and is insensitive to curare.

Animals↗
PubMed1999

Endothelial membrane potential regulates production of both nitric oxide and superoxide--a fundamental determinant of vascular health.

There is recent evidence that the membrane potential of vascular endothelium regulates not only nitric oxide (NO) synthesis, but also superoxide generation, such that hyperpolarization stimulates NO production while suppressing that of superoxide. Given that NO works in a variety of ways to inhibit atherothrombotic disease and hypertension, whereas superoxide not only vetoes the benefits of NO but also disrupts endothelial metabolism and promotes LDL oxidation through its oxidant activity, it is thus evident that endothelium membrane potential is a crucial determinant of cardiovascular risk. Membrane polarization can be enhanced by measures which increase the synthesis or availability of the Na+-K+-ATPase, moderately enhance serum K+ and increase the conductance of membrane K+ channels. Such measures may include high-K+/low-Na+ natural diets, insulin sensitizing modalities, 'euthyroid replacement therapy' and ACE inhibitors. Epidemiological correlations of insulin resistance with hypertension and cardiovascular risk may reflect the low membrane potential of insulin-resistant vascular endothelium. Adjunctive measures for suppressing the generation or half-life of endothelial superoxide are suggested.

Aldosterone↗
PubMed1992

Simultaneous fluorescence measurement of calcium and membrane potential responses to endothelin.

Vasopressin stimulates calcium signaling and chloride-dependent depolarization in glomerular mesangial cells. We describe a technique whereby both calcium and membrane potential changes can be simultaneously monitored with fluorescent probes. This technique was validated by comparison with single parameter measurements in basal and vasopressin-stimulated mesangial cells. It was shown that the calibration for calcium is unaffected by that for membrane potential, whereas the calibration for membrane potential is affected by prior calcium calibration. Accordingly, it was necessary to calibrate for the former first. The technique was then applied to investigate the effects of endothelin, which was found to elicit a concentration-dependent calcium release response and a chloride-dependent depolarization of mesangial cells. The interaction between the calcium signaling response to vasopressin and endothelin was also investigated. When vasopressin stimulation occurred subsequent to endothelin stimulation, and vice versa, a calcium response was still evident. However, these agonists displayed partial heterologous desensitization in that prior stimulation with vasopressin attenuated the subsequent response to endothelin, and vice versa. This suggests the presence of functionally distinct hormone-responsive calcium pools. The technique of double-parameter fluorescent measurement outlined could potentially be applied to other cellular signaling parameters by the use of the appropriate probes.

Animals↗