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M F Schneider

Publications and source records attributed to M F Schneider.

At least 19 recordsLinked to original sources
PubMed1997

Decay of calcium transients after electrical stimulation in rat fast- and slow-twitch skeletal muscle fibres.

1. Calcium transients were calculated from fura-2 fluorescence signals (corrected for kinetic delays in the Ca(2+)-fura-2 reaction) from single rat skeletal muscle fibres, either fully dissociated from the fast-twitch flexor digitorum brevis (FDB) muscle or in small bundles from the slow-twitch soleus muscle. Fibres or bundles were embedded in agarose gel to inhibit movement and stimulated by single or trains of 1-2 ms electrical pulses (100 Hz, 2-400 ms train duration). 2. The rate constant of decay of [Ca2+] determined from single-exponential fits to the final decay phase of [Ca2+] after a single action potential was considerably faster in FDB fibres than in soleus fibres. As the stimulation duration increased, the rate constant of [Ca2+] decay decreased for both the FDB and soleus fibres, but the effect was greater in FDB than in soleus fibres. 3. Using the magnitude of the decline in the rate constant of [Ca2+] decay with increasing stimulation duration as an index of relative contribution of the saturable Ca2+ binding sites on parvalbumin, subpopulations termed 'high', 'medium' and 'low', referring to estimated parvalbumin content, were determined within each group of FDB and soleus fibres. In fibres assigned to the 'high' and 'medium' groups, parvalbumin was the major contributor (50-73%) to the [Ca2+] decay rate constant after a single action potential. In fibres in the 'low' group, parvalbumin contributed only 0-28% to the rate constant of [Ca2+] decay. 4. Fluorescence recordings using mag-fura-2, a lower-affinity Ca2+ indicator expected to be in equilibrium with myoplasmic Ca2+, gave similar values for both the [Ca2+] decay rate constant after a single action potential and the decrease in this rate constant with increased stimulation duration, as found for the fura-2 [Ca2+] transients from FDB and soleus fibres. Thus, the observed differences in decay rate of Ca2+ were not introduced by kinetic correction of the fura-2 recordings, but are attributed to differences in the Ca2+ binding and transport properties of fast- and slow-twitch mammalian fibres.

Animals↗
PubMed1997

Release-activated Ca2+ transport in neurons of frog sympathetic ganglia.

Frog sympathetic ganglion neurons exhibit a novel Ca2+ uptake mechanism, release-activated calcium transport or RACT, which is manifest in both cytosolic and store [Ca2+] signals as greatly accelerated Ca2+ uptake after Ca2+ release from internal stores. RACT is activated by Ca2+ release but not by Ca2+ entry and serves to selectively refill Ca2+ stores after release. RACT lowers cytosolic [Ca2+] with a rate constant about 1.6 times that of the SERCA pump with empty ER. RACT is thapsigargin-insensitive, was eliminated by ryanodine, but was not affected by blocking mitochondrial or plasma membrane Ca2+ transport. A Ca2+ flux model with RACT in the ER membrane reproduced the cytosolic and store [Ca2+] responses to all stimuli.

Animals↗
PubMed1997

Calcium transients and calcium homeostasis in adult mouse fast-twitch skeletal muscle fibers in culture.

Skeletal muscle fibers enzymatically dissociated from adult mouse flexor digitorum brevis muscles were maintained in culture for up to 8 days. After various times in culture, fibers were loaded with fura 2, and Ca2+ transients for trains of 1, 5, and 10 action potentials (100 Hz) triggered by external electrical stimulation were calculated from fluorescence ratio records corrected for noninstantaneous reaction of fura 2 with Ca2+. The decay rate constants of Ca2+ transients decreased with increasing stimulation duration, indicating a slowing of the Ca(2+)-removal properties with increased stimulation duration. After 6 days in culture, Ca2+ decay rate constants decreased dramatically for all stimulation durations and the differences in decay rate constants among 1, 5, and 10 pulses became smaller. Intracellular parvalbumin content measured by single-fiber immunofluorescence decreased with time in culture in parallel with the decrease in the decay rate constant of Ca2+ transients. Our results suggest that there is a correlation between parvalbumin content and the decay rate constant of the Ca2+ transient.

Animals↗
PubMed1996

Repriming and activation alter the frequency of stereotyped discrete Ca2+ release events in frog skeletal muscle.

1. Brief localized elevations in myoplasmic [Ca2+] (Ca2+ sparks) in individual sarcomeres of voltage-clamped frog skeletal muscle fibres were examined by laser scanning confocal microscopy. 2. Fibres held at 0 mV were briefly repolarized to -90 mV (repriming pulse) to restore only a small fraction of sarcoplasmic reticulum (SR) calcium release. Subsequent depolarization to 0 mV (test pulse) caused the appearance of small numbers of Ca2+ sparks at different sarcomeres from pulse to pulse. Increasing the repriming time resulted in an increase in the frequency of occurrence of the Ca2+ sparks. 3. The amplitude and spatio-temporal extent of the Ca2+ sparks were independent of the repriming time and test pulse voltage. Ca2+ sparks recorded during small depolarizations of fibres held at -90 mV had a similar amplitude and spatio-temporal extent as those recorded after brief repriming of the same fibre held at 0 mV. 4. We conclude that stereotyped Ca2+ sparks underlie calcium release at all voltages and all extents of repriming. The amplitude of Ca2+ release is thus graded by the frequency but not by the amplitude or spatio-temporal extent of the individual SR Ca2+ release events.

Animals↗
PubMed1996

Two mechanisms of quantized calcium release in skeletal muscle.

Skeletal muscle uses voltage sensors in the transverse tubular membrane that are linked by protein-protein interactions to intracellular ryanodine receptors, which gate the release of calcium from the sarcoplasmic reticulum. Here we show, by using voltage-clamped single fibres and confocal imaging, that stochastic calcium-release events, visualized as Ca2+ sparks, occur in skeletal muscle and originate at the triad. Unitary triadic Ca(2+)-release events are initiated by the voltage sensor in a steeply voltage-dependent manner, or occur spontaneously by a mechanism independent of the voltage sensor. Large-amplitude events also occur during depolarization and consist of two or more unitary events. We propose a 'dual-control' model for discrete Ca2+ release events from the sacroplasmic reticulum that unifies diverse observations about Ca(2+)-signalling in frog skeletal muscle, and that may be applicable to other excitable cells.

Animals↗
PubMed1996

Sarcomeric calcium sparks activated by fiber depolarization and by cytosolic Ca2+ in skeletal muscle.

Discrete highly localized elevations of myoplasmic [Ca2+], calcium 'sparks', have been detected in skeletal muscle fibers. During relatively small depolarizations of a fiber, the calcium sparks are several times larger than the average increase in [Ca2+] and can thus be clearly resolved. The spark event frequency increases steeply with increasing depolarization, so that for larger depolarizations the discrete microscopic [Ca2+] elevations blend together and become indistinguishable in the average macroscopic [Ca2+] transient. Spontaneous calcium sparks also occur in the absence of voltage sensor activity, in which case they are activated by myoplasmic Ca2+. Both the voltage-activated and Ca(2+)-activated events originate at the location of the triad within the sarcomere. Calcium sparks appear to constitute the elementary unit of calcium release activation in skeletal muscle.

Animals↗
PubMed1995

Suppression of calcium release by calcium or procaine in voltage clamped rat skeletal muscle fibres.

1. Calcium transients were measured in fast-twitch rat skeletal muscle fibres stretched to 3.7-4.0 microns per sarcomere, and voltage clamped at a holding potential of -80 mV using the double-seal Vaseline gap technique. Resting calcium was monitored with fura-2 and the calcium transients were measured with antipyrylazo III. The rate of release of calcium from the sarcoplasmic reticulum was calculated from the calcium transient records. The temperature was 14-17 degrees C. 2. The steady-state calcium dependence of inactivation of release was studied with a two-pulse protocol in which 200 ms prepulses of different amplitudes elevated the internal calcium concentration to various levels. The inactivation of release was then measured in the test pulse that followed the prepulses. The calcium concentration at which the inactivation of release are half-maximal was approximately 0.22 microM, the average number of bound calcium ions needed to cause inactivation was about three per release channel and the amount of release that could be inactivated was, on average, 2.48 times the steady level of release during the test pulses. 3. Procaine (0.3mM) reversibly decreased the amplitude and the rate of rise of the calcium transient. Both the peak and the steady level of release were decreased by about 50%. The shape of the release waveform was not modified.

Animals↗
PubMed1995

Direct involvement of intracellular Ca2+ transport ATPase in the development of thapsigargin resistance by Chinese hamster lung fibroblasts.

Thapsigargin (TG), a specific inhibitor of intracellular Ca2+ transport ATPases (SERCA), inhibits cell proliferation when added to culture media in the nanomolar concentration range. However, long term exposure to gradually increasing concentrations of TG induces resistance to TG inhibition in both the parental Chinese hamster lung fibroblast DC-3F and a subline derived from it via transfection and stable expression of a full-length cDNA encoding avian SERCA1 ATPase (DC-3F/Ca cells). TG resistance develops in parallel with selection of cells expressing higher levels of the endogenous SERCA2 as well as of the exogenous transfected SERCA1 ATPase, whose Ca2+ transport function can be studied in situ by imaging techniques and following isolation in microsomal fractions. Microsomes isolated from resistant cells contain two functionally distinct populations of ATPases: a population that is inhibited by stoichiometric titration with TG, and a population displaying resistance to inhibition even when TG exceeds the enzyme stoichiometry. It is apparent that resistance to TG develops in parallel with (a) selection of cells expressing high levels of SERCA ATPases, and (b) selection of an ATPase that is resistant to TG.

Animals↗
PubMed1995

Calcium transients in intact rat skeletal muscle fibers in agarose gel.

Intact single fibers enzymatically dissociated from rat flexor digitorum brevis muscle were suspended in 0.5% low-melting-temperature agarose gel to minimize fiber movement during action potentials or trains of action potentials. Resting Ca2+ concentration ([Ca2+]) and changes in [Ca2+] were monitored using the fluorescent calcium indicator fura 2. The time course and waveform of [Ca2+] transients during an action potential or trains of action potentials in fibers in agarose were calculated using kinetic parameters previously determined to correct for the calcium-fura 2 kinetic delay. Half times of the calculated calcium transients for single action potentials were 30-fold briefer than the original fura 2 signals. To confirm the time course and waveform of the calculated calcium transients, changes in [Ca2+] were monitored using the more rapidly equilibrating calcium indicator mag-fura 2. [Ca2+] transients for fibers containing fura 2 had very similar time courses and waveforms as mag-fura 2 signals from other fibers, indicating that the corrections for the calcium-fura 2 kinetic delay were accurate. The advantages of the agarose gel suspension are discussed.

Action Potentials↗
PubMed1993

Inositol 1,4,5-trisphosphate-mediated quantal Ca2+ release measured by high resolution imaging of Ca2+ within organelles.

The distribution and operation of Ca2+ pools within cells has been directly studied in situ by monitoring the Ca2+ inside Ca2+ dye-loaded organelles using high resolution imaging procedures. Using DDT1MF-2 smooth muscle cells, loaded with fura-2 under conditions favoring dye entry into organelles and subjected to carefully controlled permeabilization still attached to coverslips, the Ca2+ within organelles was analyzed by high resolution, z axis-controlled imaging, and deblurring methods. Saturation analysis of entrapped fura-2 indicated that the dye reported Ca2+ identically to fura-2 in solution. Areas containing high Ca(2+)-sequestering organelles (> 5 microM free Ca2+) were observed to predominate around the nucleus and close to the periphery of the cell. Analysis of the actions of inositol 1,4,5-trisphosphate (InsP3) within small (3 microns 2) selected intracellular areas, revealed a "quantal" release phenomenon, with rapid attainment of limited stable release at submaximal InsP3 levels. The apparent EC50 for InsP3 was approximately 3 microns, higher than within suspensions of permeabilized cells. The action of InsP3 was competitively blocked by 10 micrograms/ml of the InsP3 antagonist, heparin. Applied after maximal InsP3-mediated Ca2+ release, heparin reversed InsP3-induced Ca2+ release resulting in reuptake of Ca2+ into Ca(2+)-pumping organelles with identical spatial distribution as before Ca2+ release. InsP3 released Ca2+ from all areas of high Ca(2+)-pumping organelles; extensive areas of high fura-2-loading, but low intraorganelle Ca2+, were unchanged by InsP3. GTP induced no alteration in Ca2+ release (in contrast to suspensions of permeabilized cells), suggesting that the InsP3-sensitive Ca2+ pool was functioning as a single homogeneous pool. Opening of InsP3-sensitive channels was also monitored by assessing InsP3-activated channel-mediated Mn2+ quenching of organelle-loaded fura-2; the results revealed a similar pattern of quantal release, with slightly increased apparent InsP3 sensitivity. The results provide the first high resolution in situ localization of Ca2+ signaling organelles and demonstrate the quantal operation of InsP3-sensitive Ca2+ pools within highly discrete subcellular loci.

Animals↗
PubMed1993

Microinjection of strong calcium buffers suppresses the peak of calcium release during depolarization in frog skeletal muscle fibers.

The effects of high intracellular concentrations of various calcium buffers on the myoplasmic calcium transient and on the rate of release of calcium (Rrel) from the sarcoplasmic reticulum (SR) were studied in voltage-clamped frog skeletal muscle fibers. The changes in intracellular calcium concentration (delta[Ca2+]) for 200-ms pulses to 0-20 mV were recorded before and after the injection of the calcium buffer and the underlying Rrel was calculated. If the buffer concentration after the injection was high, the initial rate of rise of the calcium transient was slower after injection than before and was followed by a slow increase of [Ca2+] that resembled a ramp. The increase in myoplasmic [Mg2+] that accompanies the calcium transient in control was suppressed after the injection and a slight decrease was observed instead. After the injection the buffer concentration in the voltage-clamped segment of the fiber decreased as the buffer diffused away toward the open ends. The calculated apparent diffusion coefficient for fura-2 (Dapp = 0.40 +/- 0.03 x 10(-6) cm2/s, mean +/- SEM, n = 6) suggests that approximately 65-70% of the indicator was bound to relatively immobile intracellular constituents. As the concentration of the injected buffer decreased, the above effects were reversed. The changes in delta[Ca2+] were underlined by characteristic modification of Rrel. The early peak component was suppressed or completely eliminated; thus, Rrel rose monotonically to a maintained steady level if corrected for depletion. If Rrel was expressed as percentage of SR calcium content, the steady level after injection did not differ significantly from that before. Control injections of anisidine, to the concentration that eliminated the peak of Rrel when high affinity buffers were used, had only a minor effect on Rrel, the peak was suppressed by 26 +/- 5% (mean +/- SE, n = 6), and the steady level remained unchanged. Thus, the peak component of Rrel is dependent on a rise in myoplasmic [Ca2+], consistent with calcium-induced calcium release, whereas the steady component of Rrel is independent of myoplasmic [Ca2+].

Animals↗
PubMed1993

Calcium transients and calcium release in rat fast-twitch skeletal muscle fibres.

1. Calcium transients were recorded from cut segments of fast-twitch rat skeletal muscle fibres stretched to 3.7-4.0 microns per sarcomere and voltage clamped at a holding potential of -80 mV using the double Vaseline-gap technique. Calcium transients were monitored simultaneously with the two calcium indicators antipyrylazo III (AP III) and fura-2. AP III was used to record the calcium changes in response to 10-200 ms depolarizing pulses to different membrane potentials while fura-2 monitored the slow decay of the transient (during 16-20 s) and the resting calcium concentration. Experiments were performed at 14-17 degrees C. 2. For 50-100 ms depolarizing pulses calcium transients were first detected between -30 and -20 mV in a total of twenty-one fibres. The transients recorded with AP III showed a plateau for small pulses (-20 mV) and a steady increase during stronger pulses (-10 mV and more positive). Upon repolarization the transients decayed towards the baseline. The signal recorded simultaneously with fura-2 showed a continuous increase of the transient during the pulses at all membrane potentials. The amplitude of the calcium transients for the large pulses could not be followed with fura-2 due to saturation of the dye. 3. The signals obtained with both dyes were used to determine the kinetics of the calcium-fura-2 reaction inside the fibres. The mean values of the kinetic parameters were: the on rate constant (kon) = 5.1 x 10(8) M-1s-1, the off rate constant (koff) = 26 s-1, and koff/kon (KD) = 69.7 nM. 4. The fast phase of decay of the calcium transients after the pulses was studied from the records obtained with AP III. For depolarizing pulses of the same duration, the rate of decay of the transients after the pulse was slower the stronger the depolarization. For pulses to the same membrane potential, the rate of decay was slower the longer the pulse duration. Both stimulating patterns indicated saturation of the removal system in the muscle fibres due to occupancy of slowly equilibrating myoplasmic calcium binding sites by released calcium. 5. The fast phase of decay of the signals obtained with AP III was well fitted with a model of the system for removing calcium from the myofilament space. 6. The rate of calcium release (Rrel) from the sarcoplasmic reticulum was calculated once the removal system was characterized in the same fibre.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

IP3 receptor: localization to plasma membrane of T cells and cocapping with the T cell receptor.

Immune responses in lymphocytes require cellular accumulation of large amounts of calcium (Ca2+) from extracellular sources. In the T cell tumor line Jurkat, receptors for the Ca(2+)-releasing messenger inositol 1,4,5-trisphosphate (IP3) were localized to the plasma membrane (PM). Capping of the T cell receptor-CD3 complex, which is associated with signal transduction, was accompanied by capping of IP3 receptors. The IP3 receptor on T cells appears to be responsible for the entry of Ca2+ that initiates proliferative responses.

Antigens, CD↗
PubMed1992

Depolarization-induced calcium release from isolated triads measured with impermeant fura-2.

Depolarization-induced Ca2+ release was studied in a mixture of triads and terminal cisternae isolated from rabbit skeletal muscle. The vesicles were actively loaded with known amounts of Ca2+ in the absence of precipitating anions in a solution containing 100 mM K propionate buffer. Changes in extravesicular Ca2+ were monitored with 10 microM Fura-2 (membrane impermeant form). Ca2+ release was initiated by diluting an aliquot of the loaded vesicles into a TEACl release solution designed to maintain a constant [K+].[Cl-] product. Fast release, defined as the percentage of total Ca2+ loaded which released in less than 10 sec, occurred when extravesicular free Ca2+ was in the submicromolar range and was unaffected by 5 mM caffeine under depolarizing conditions, change in external pH to 6.5, and an increase in external Mg2+ concentration from 0.1 to 0.2 mM. Thus, the Ca2+ release measured in these studies is distinct from Ca(2+)-induced Ca2+ release. The fast release more than doubled when a greater dilution (1:20 versus 1:10) of the loaded vesicles into the release solution, which would produce a larger depolarization, was used. The percentage of loaded Ca2+ which released rapidly in a particular triad preparation was similar to the percentage of vesicles structurally coupled as visualized by electron microscopy.

Animals↗
PubMed1992

Effects of low myoplasmic Mg2+ on calcium binding by parvalbumin and calcium uptake by the sarcoplasmic reticulum in frog skeletal muscle.

The effects of low intracellular free Mg2+ on the myoplasmic calcium removal properties of skeletal muscle were studied in voltage-clamped frog skeletal muscle fibers by analyzing the changes in intracellular calcium and magnesium due to membrane depolarization under various conditions of internal free [Mg2+]. Batches of fibers were internally equilibrated with cut end solutions containing two calcium indicators, antipyrylazo III (AP III) and fura-2, and different concentrations of free Mg2+ (25 microM-1 mM) obtained by adding appropriate total amounts of ATP and magnesium to the solutions. Changes in AP III absorbance were used to monitor [Ca2+] and [Mg2+] transients, whereas fura-2 fluorescence was mostly used to monitor resting [Ca2+]. Shortly after applying an internal solution containing less than 60 microM free Mg2+ to the cut ends of depolarized fibers most of the fibers exhibited spontaneous repetitive movements, suggesting that free internal Mg2+ might affect the activity of the sarcoplasmic reticulum (SR) calcium channels at rest. The spontaneous contractions generally subsided. In polarized fibers the maximal amplitude of the calcium transient elicited by a depolarizing pulse was about the same whatever the internal [Mg2+], but its decay after the end of the pulse slower in low [Mg2+]. In low [Mg2+] (less than 0.14 mM), the mean rate constant of decay obtained from fitting a single exponential plus a constant to the decay of the calcium transients was approximately 30% of its value in the control fibers (1 mM internal [Mg2+]). A model characterizing the main calcium removal properties of a frog skeletal muscle fiber, including the SR pump and the Ca-Mg sites on parvalbumin, was fitted to the decay of the calcium transients. Results of the fits show that in low internal [Mg2+] the slowing of the decay of the calcium transient can be well predicted by both a decreased rate of SR calcium uptake and an expected decreased resting magnesium occupancy of parvalbumin leading to a reduced contribution of parvalbumin to the overall rate of calcium removal. These results are thus consistent with the known properties of parvalbumin as a Ca-Mg buffer and furthermore suggest that in an intact portion of a muscle fiber, the activity of the SR calcium pump can be affected by the level of free Mg2+.

Animals↗
PubMed1992

Low myoplasmic Mg2+ potentiates calcium release during depolarization of frog skeletal muscle fibers.

The role of intracellular free magnesium concentration ([Mg2+]) in modulating calcium release from the sarcoplasmic reticulum (SR) was studied in voltage-clamped frog cut skeletal muscle fibers equilibrated with cut end solutions containing two calcium indicators, fura-2 and antipyrylazo III (AP III), and various concentrations of free Mg2+ (25 microM-1 mM) obtained by adding appropriate total amounts of ATP and magnesium to the solutions. Changes in AP III absorbance were used to monitor calcium transients, whereas fura-2 fluorescence was used to monitor resting calcium. The rate of release (Rrel) of calcium from the SR was calculated from the calcium transient and found to be increased in low internal [Mg2+]. After correcting for effects of calcium depletion from the SR and normalization to SR content, the mean values of the inactivatable and noninactivatable components of Rrel were increased by 163 and 46%, respectively, in low Mg2+. Independent of normalization to SR content, the ratio of inactivatable to noninactivatable components of Rrel was increased in low internal [Mg2+]. Both observations suggest that internal [Mg2+] preferentially modulates the inactivatable component of Rrel, which is thought to be due to calcium-induced calcium release from the SR. This could also explain the observation that, in low internal [Mg2+], the time to the peak of the calcium transient for a 5-ms depolarizing pulse was not very different from the time to the peak of the delta [Ca2+] for a 10-ms pulse of the same amplitude. Finally, in low internal [Mg2+], the calcium transient elicited by a short depolarizing pulse was in some cases clearly followed by a very slow rise of calcium after the end of the pulse. The observed effects of reduced [Mg2+] on calcium release are consistent with a removal of the inhibition that the normal 1 mM myoplasmic [Mg2+] exerts on calcium release in skeletal muscle fibers.

Animals↗
PubMed1992

Effects of procaine and caffeine on calcium release from the sarcoplasmic reticulum in frog skeletal muscle.

1. Resting myoplasmic free [Ca2+] and [Ca2+] transients (delta [Ca2+]) were measured in single voltage-clamped frog skeletal muscle fibres in the presence and absence of procaine, caffeine or procaine plus caffeine using Fura-2 fluorescence and antipyrylazo III (Ap III) absorbance signals. The rate of release (Rrel) of calcium from the sarcoplasmic reticulum (SR) was calculated from the calcium transients and corrected for the relatively small decline due to depletion of calcium from the SR. 2. Procaine (1 mM) reversibly suppressed delta [Ca2+] and the corresponding Rrel by about 40% for 60-100 ms depolarizing steps to -40 to +20 mV. Procaine had little effect on either the waveform or voltage dependence of the Rrel records. 3. [Ca2+] transients calculated from Fura-2 fluorescence changes in the presence or absence of procaine had similar time courses and amplitudes as those calculated from the Ap III absorbance changes suggesting that 1 mM-procaine did not interfere with the ability of Ap III or Fura-2 to monitor delta [Ca2+]. 4. Although 1 mM-procaine depressed Rrel it had no effect on intramembrane charge movements (IQ) calculated from membrane currents recorded simultaneously with delta [Ca2+]. 5. Procaine (1 mM) reversibly inhibited the potentiating effect of 0.5 mM-caffeine on delta [Ca2+]. The amplitude and waveform of the Rrel records were similar in control fibres and in the presence of 1 mM-procaine plus 0.5 mM-caffeine. 6. In the presence of 0.5 mM-caffeine delta [Ca2+] after 10-20 ms voltage steps exhibited an increase in the time to peak and a slower decay time course compared with caffeine-free controls, suggestive of significant calcium-induced calcium release in the presence of caffeine. These effects of caffeine were completely and reversibly blocked by 1 mM-procaine. 7. In the absence of caffeine, 1 mM-procaine caused a small decrease in time to peak of delta [Ca2+] after 10-30 ms duration voltage steps compared to the bracketing control and wash runs without procaine. Rrel turned off faster after 10 ms pulses in procaine than in the absence of procaine, but the turn-off of release was about equally fast with or without procaine after pulses of 20 ms or longer. The effect of procaine after 10 ms pulses in the absence of caffeine may indicate suppression of a component of calcium-induced calcium release in control that inactivates during the pulse.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗