Effects of Na+/Ca2+ exchanger downregulation on contractility and [Ca2+]i transients in adult rat myocytes

2002 ◽  
Vol 283 (4) ◽  
pp. H1616-H1626 ◽  
Author(s):  
George M. Tadros ◽  
Xue-Qian Zhang ◽  
Jianliang Song ◽  
Lois L. Carl ◽  
Lawrence I. Rothblum ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Current Density ◽  
Resting Membrane Potential ◽  
Action Potential Amplitude ◽  
Half Time ◽  
Adult Rat ◽  
Postmyocardial Infarction ◽  
Intracellular Ca ◽  
Rat Myocytes

Postmyocardial infarction (MI) rat myocytes demonstrated depressed Na+/Ca2+exchange (NCX1) activity, altered contractility, and intracellular Ca2+ concentration ([Ca2+]i) transients. We investigated whether NCX1 downregulation in normal myocytes resulted in contractility changes observed in MI myocytes. Myocytes infected with adenovirus expressing antisense (AS) oligonucleotides to NCX1 had 30% less NCX1 at 3 days and 66% less NCX1 at 6 days. The half-time of relaxation from caffeine-induced contracture was twice as long in ASNCX1 myocytes. Sarcoplasmic reticulum (SR) Ca2+-ATPase abundance, SR Ca2+uptake, resting membrane potential, action potential amplitude and duration, L-type Ca2+ current density and cell size were not affected by ASNCX1 treatment. At extracellular Ca2+ concentration ([Ca2+]o) of 5 mM, ASNCX1 myocytes had significantly lower contraction and [Ca2+]i transient amplitudes and SR Ca2+ contents than control myocytes. At 0.6 mM [Ca2+]o, contraction and [Ca2+]i transient amplitudes and SR Ca2+ contents were significantly higher in ASNCX1 myocytes. At 1.8 mM [Ca2+]o, contraction and [Ca2+]i transient amplitudes were not different between control and ASNCX1 myocytes. This pattern of contractile and [Ca2+]i transient abnormalities in ASNCX1 myocytes mimics that observed in rat MI myocytes. We conclude that downregulation of NCX1 in adult rat myocytes resulted in decreases in both Ca2+ influx and efflux during a twitch. We suggest that depressed NCX1 activity may partly account for the contractile abnormalities after MI.

A discrete Na-Ca exchange-dependent Ca compartment in rat ventricular cells: exchange and localization

1992 ◽  
Vol 262 (5) ◽  
pp. C1149-C1153 ◽  
Author(s):  
G. A. Langer ◽  
T. L. Rich
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Binding Sites ◽  
Rat Heart ◽  
Half Time ◽  
Adult Rat ◽  
Ventricular Cells ◽  
Intracellular Ca ◽  
Rapid Perfusion ◽  
Limited Exchange

Application of a new rapid perfusion (up to 4.8 ml/s) technique to 45Ca-labeled ventricular cells from adult rat heart has defined a discrete intracellular calcium (Ca) compartment with the following characteristics: 1) its exchange is absolutely dependent on operation of the Na-Ca exchanger, i.e., its isotopic content remains constant during washout in the absence of Na and Ca and is released only upon addition of Na and Ca to the perfusate. 2) At an extracellular Ca concentration of 1.0 mM it contains 350 mumol/kg dry wt cells and exchanges with half time of 650 ms. Ca flux from the compartment is 385 mumol.kg dry wt-1.s-1 or 20% of the total nonperfusion limited flux from the cells. 3) Its content is decreased 19% by 10 mM caffeine but not diminished by exposure of the cells to 10(-6) M ryanodine and not accessible to lanthanum (La) displacement. 4) Only limited exchange occurs when only Na or Ca is present and exchange is virtually eliminated by substitution of extracellular Li for extracellular Na. 5) Replacement of Na and Ca to the perfusate after various periods of removal produces no contraction (despite immediate Ca release from the cell). The results define a discrete intracellular Ca compartment which exchanges only via the Na-Ca exchanger. It is not La accessible, not in the ryanodine- or caffeine-sensitive portions of the sarcoplasmic reticulum, not in the mitochondria nor at the myofilaments, but may reside at inner sarcolemmal leaflet binding sites.

scholarly journals Effects of impaired Ca2+homeostasis on contraction in postinfarction myocytes

1999 ◽  
Vol 86 (3) ◽  
pp. 943-950 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Timothy I. Musch ◽  
Robert Zelis ◽  
Joseph Y. Cheung
Keyword(s):  
Myocardial Infarction ◽  
Steady State ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Mechanical Activity ◽  
Half Time ◽  
Rat Hearts ◽  
Rat Myocytes ◽  
State Contraction ◽  
Exchange Activity

The significance of altered Ca2+ influx and efflux pathways on contractile abnormalities of myocytes isolated from rat hearts 3 wk after myocardial infarction (MI) was investigated by varying extracellular Ca2+concentration ([Ca2+]o, 0.6–5.0 mM) and pacing frequency (0.1–5.0 Hz). Myocytes isolated from 3-wk MI hearts were significantly longer than those from sham-treated (Sham) hearts (125 ± 1 vs. 114 ± 1 μm, P < 0.0001). At high [Ca2+]oand low pacing frequency, conditions that preferentially favored Ca2+ influx over efflux, Sham myocytes shortened to a greater extent than 3-wk MI myocytes. Conversely, under conditions that favored Ca2+ efflux (low [Ca2+]oand high pacing frequency), MI myocytes shortened more than Sham myocytes. At intermediate [Ca2+]oand pacing frequencies, differences in steady-state contraction amplitudes between Sham and MI myocytes were no longer significant. Collectively, the interpretation of these data was that Ca2+ influx and efflux pathways were subnormal in MI myocytes and that they contributed to abnormal cellular contractile behavior. Because Na+/Ca2+exchange activity, but not whole cell Ca2+ current, was depressed in 3-wk MI rat myocytes, our results on steady-state contraction are consistent with, but not proof of, the hypothesis that depressed Na+/Ca2+exchange accounted for abnormal contractility in MI myocytes. The effects of depressed Na+/Ca2+exchange on MI myocyte mechanical activity were further evaluated in relaxation from caffeine-induced contractures. Because Ca2+ uptake by sarcoplasmic reticulum was inhibited by caffeine and with the assumption that intracellular Na+ and membrane potential were similar between Sham and MI myocytes, myocyte relaxation from caffeine-induced contracture can be taken as an estimate of Ca2+ extrusion by Na+/Ca2+exchange. In MI myocytes, in which Na+/Ca2+exchange activity was depressed, the half time of relaxation (1.54 ± 0.14 s) was significantly ( P < 0.02) prolonged compared with that measured in Sham myocytes (1.10 ± 0.10 s).

In situ SR function in postinfarction myocytes

1999 ◽  
Vol 87 (6) ◽  
pp. 2143-2150 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Russell L. Moore ◽  
Timothy I. Musch ◽  
Joseph Y. Cheung
Keyword(s):  
Myocardial Infarction ◽  
Sarcoplasmic Reticulum ◽  
Half Time ◽  
Time Constants ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes ◽  
Electrophysiological Technique ◽  
Empirical Constants

Previous studies have shown lower systolic intracellular Ca2+ concentrations ([Ca2+]i) and reduced sarcoplasmic reticulum (SR)-releasable Ca2+ contents in myocytes isolated from rat hearts 3 wk after moderate myocardial infarction (MI). Ca2+ entry via L-type Ca2+ channels was normal, but that via reverse Na+/Ca2+exchange was depressed in 3-wk MI myocytes. To elucidate mechanisms of reduced SR Ca2+ contents in MI myocytes, we measured SR Ca2+uptake and SR Ca2+ leak in situ, i.e., in intact cardiac myocytes. For sham and MI myocytes, we first demonstrated that caffeine application to release SR Ca2+ and inhibit SR Ca2+ uptake resulted in a 10-fold prolongation of half-time ( t ½) of [Ca2+]itransient decline compared with that measured during a normal twitch. These observations indicate that early decline of the [Ca2+]itransient during a twitch in rat myocytes was primarily mediated by SR Ca2+-ATPase and that the t ½ of [Ca2+]idecline is a measure of SR Ca2+uptake in situ. At 5.0 mM extracellular Ca2+, systolic [Ca2+]iwas significantly ( P ≤ 0.05) lower (337 ± 11 and 416 ± 18 nM in MI and sham, respectively) and t ½ of [Ca2+]idecline was significantly longer (0.306 ± 0.014 and 0.258 ± 0.014 s in MI and sham, respectively) in MI myocytes. The 19% prolongation of t ½ of [Ca2+]i decline was associated with a 23% reduction in SR Ca2+-ATPase expression (detected by immunoblotting) in MI myocytes. SR Ca2+ leak was measured by a novel electrophysiological technique that did not require assigning empirical constants for intracellular Ca2+buffering. SR Ca2+ leak rate was not different between sham and MI myocytes: the time constants of SR Ca2+ loss after thapsigargin were 290 and 268 s, respectively. We conclude that, independent of decreased SR filling by Ca2+ influx, the lower SR Ca2+ content in MI myocytes was due to reduced SR Ca2+ uptake and SR Ca2+-ATPase expression, but not to enhanced SR Ca2+ leak.

Sprint training normalizes Ca2+ transients and SR function in postinfarction rat myocytes

2000 ◽  
Vol 89 (1) ◽  
pp. 38-46 ◽  
Author(s):  
Lian-Qin Zhang ◽  
Xue-Qian Zhang ◽  
Yuk-Chow Ng ◽  
Lawrence I. Rothblum ◽  
Timothy I. Musch ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Sarcoplasmic Reticulum ◽  
Contractile Function ◽  
Half Time ◽  
Sprint Training ◽  
Cardiac Contractile Function ◽  
Cardiac Contractile ◽  
Rat Hearts ◽  
Intracellular Ca ◽  
Rat Myocytes

Previous studies have shown that myocytes isolated from sedentary (Sed) rat hearts 3 wk after myocardial infarction (MI) undergo hypertrophy, exhibit altered intracellular Ca2+ concentration ([Ca2+]i) dynamics and abnormal contraction, and impaired sarcoplasmic reticulum (SR) function manifested as prolonged half-time of [Ca2+]idecline. Because exercise training elicits positive adaptations in cardiac contractile function and myocardial Ca2+ regulation, the present study examined whether 6–8 wk of high-intensity sprint training (HIST) would restore [Ca2+]i dynamics and SR function in MI myocytes toward normal. In MI rats, HIST ameliorated myocyte hypertrophy as indicated by significant ( P ≤ 0.05) decreases in whole cell capacitances [Sham-Sed 179 ±12 ( n = 20); MI-Sed 226 ± 7 ( n = 20); MI-HIST 183 ± 11 pF ( n = 19)]. HIST significantly ( P < 0.0001) restored both systolic [Ca2+]i [Sham-Sed 421 ± 9 ( n = 79); MI-Sed 350 ± 6 ( n = 70); MI-HIST 399 ± 9 nM ( n = 70)] and half-time of [Ca2+]i decline (Sham-Sed 0.197 ± 0.005; MI-Sed 0.247 ± 0.006; MI-HIST 0.195 ± 0.006 s) toward normal. Compared with Sham-Sed myocytes, SR Ca2+-ATPase expression significantly ( P < 0.001) decreased by 44% in MI-Sed myocytes. Surprisingly, expression of SR Ca2+-ATPase was further reduced in MI-HIST myocytes to 26% of that measured in Sham-Sed myocytes. There were no differences in calsequestrin expression among the three groups. Expression of phospholamban was not different between Sham-Sed and MI-Sed myocytes but was significantly ( P < 0.01) reduced in MI-HIST myocytes by 25%. Our results indicate that HIST instituted shortly after MI improves [Ca2+]idynamics in surviving myocytes. Improvement in SR function by HIST is mediated not by increased SR Ca2+-ATPase expression, but by modulating phospholamban regulation of SR Ca2+-ATPase activity.

Effect of aminophylline on the contraction threshold of rat diaphragm fibers

1991 ◽  
Vol 71 (4) ◽  
pp. 1409-1414 ◽  
Author(s):  
A. S. Losavio ◽  
B. A. Kotsias
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Resting Membrane Potential ◽  
Dependent Manner ◽  
Direct Visualization ◽  
Rat Diaphragm ◽  
Current Clamp ◽  
Cyclic Monophosphate ◽  
Dose Dependent

We studied the effect of aminophylline (0.1–1 mM) on the contraction threshold (CT) of rat diaphragm fibers (25 degrees C). The CT was measured by direct visualization (x200) of the fiber under current-clamp conditions. The main findings are the following: 1) Aminophylline lowers the CT, in a dose-dependent manner, toward more negative values of the resting membrane potential (Vm). 2) Dibutyryl adenosine 3′,5′-cyclic monophosphate (2 mM) shifts the CT, although this change is smaller than in the presence of xanthine. 3) Tetracaine (1 mM), a drug that diminishes Ca release from the sarcoplasmic reticulum, reduces the shift induced by 1 mM aminophylline; this is partially overcome by increasing aminophylline concentration to 5 mM. 4) Hyperpolarization of the fibers shifts the CT to more negative Vm. We suggest that the displacement in the CT to more negative Vm plays an important role in the potentiating effect of aminophylline. This could be the result of an enhancement of Ca release from the sarcoplasmic reticulum.

scholarly journals Effects of sprint training on contractility and [Ca2+]i transients in adult rat myocytes

2002 ◽  
Vol 93 (4) ◽  
pp. 1310-1317 ◽  
Author(s):  
Xue-Qian Zhang ◽  
Jianliang Song ◽  
Lois L. Carl ◽  
Weixing Shi ◽  
Anwer Qureshi ◽  
...  
Keyword(s):  
Contractile Function ◽  
Sprint Training ◽  
Cell Width ◽  
Western Blots ◽  
Adult Rat ◽  
Protein Levels ◽  
Intracellular Ca ◽  
Uptake Activity ◽  
Rat Myocytes ◽  
Myocyte Contractility

The effects of 6–8 wk of high-intensity sprint training (HIST) on rat myocyte contractility and intracellular Ca2+ concentration ([Ca2+]i) transients were investigated. Compared with sedentary (Sed) myocytes, HIST induced a modest (5%) but significant ( P < 0.0005) increase in cell length with no changes in cell width. In addition, the percentage of myosin heavy chain α-isoenzyme increased significantly ( P < 0.02) from 0.566 ± 0.077% in Sed rats to 0.871 ± 0.006% in HIST rats. At all three (0.6, 1.8, and 5 mM) extracellular Ca2+concentrations ([Ca2+]o) examined, maximal shortening amplitudes and maximal shortening velocities were significantly ( P < 0.0001) lower and half-times of relaxation were significantly ( P < 0.005) longer in HIST myocytes. HIST myocytes had significantly ( P < 0.0001) higher diastolic [Ca2+]i levels. Compared with Sed myocytes, systolic [Ca2+]ilevels in HIST myocytes were higher at 0.6 mM [Ca2+]o, similar at 1.8 mM [Ca2+]o, and lower at 5 mM [Ca2+]o. The amplitudes of [Ca2+]i transients were significantly ( P < 0.0001) lower in HIST myocytes. Half-times of [Ca2+]i transient decline, an estimate of sarcoplasmic reticulum (SR) Ca2+ uptake activity, were not different between Sed and HIST myocytes. Compared with Sed hearts, Western blots demonstrated a significant ( P < 0.03) threefold decrease in Na+/Ca2+ exchanger, but SR Ca2+-ATPase and calsequestrin protein levels were unchanged in HIST hearts. We conclude that HIST effected diminished myocyte contractile function and [Ca2+]itransient amplitudes under the conditions studied. We speculate that downregulation of Na+/Ca2+ exchanger may partly account for the decreased contractility in HIST myocytes.

Influence of age and run training on cardiac Na+/Ca2+ exchange

2003 ◽  
Vol 95 (5) ◽  
pp. 1994-2003 ◽  
Author(s):  
Lisa C. Mace ◽  
Bradley M. Palmer ◽  
David A. Brown ◽  
Korinne N. Jew ◽  
Joshua M. Lynch ◽  
...  
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Left Ventricular ◽  
Brown Norway ◽  
Resting Membrane Potential ◽  
Whole Cell Patch Clamp ◽  
Age Related ◽  
Intracellular Ca ◽  
Whole Heart ◽  
Exchange Activity

Effects of age and training on myocardial Na+/Ca2+ exchange were examined in young sedentary (YS; 14-15 mo), aged sedentary (AS; 27-31 mo), and aged trained (AT; 8- to 11-wk treadmill run training) male Fischer Brown Norway rats. Whole heart performance and isolated cardiocyte Na+/Ca2+ exchange characteristics were measured. At the whole heart level, a small but significant slowing of late isovolumic left ventricular (LV) relaxation, which may be indicative of altered Na+/Ca2+ exchange activity, was seen in hearts from AS rats. This subtle impairment in relaxation was not observed in hearts from AT rats. At the single-cardiocyte level, late action potential duration was prolonged, resting membrane potential was more positive, and overshoot potential was greater in cardiocytes from AS rats than from YS rats ( P < 0.05). Training did not influence any of these age-related action potential characteristics. In electrically paced cardiocytes, neither shortening nor intracellular Ca2+ concentration ([Ca2+]i) dynamics was influenced by age or training. Similarly, neither age nor training influenced the rate of [Ca2+]i clearance via forward (Nain+ /Caout2+) Na+/Ca2+ exchange after caffeine-induced Ca2+ release from the sarcoplasmic reticulum or cardiac Na+/Ca2+ exchanger protein (NCX1) expression. However, when whole cell patch-clamp techniques combined with fluorescence microscopy were used to evaluate the ability of Na+/Ca2+ exchange to alter cytosolic [Ca2+] ([Ca2+]c) under conditions where membrane potential ( Vm) and internal and external [Na+] and [Ca2+] could be controlled, we observed age-associated increases in forward Na+/Ca2+ exchange-mediated [Ca2+]c clearance ( P < 0.05) that were not influenced by training. The age-related increase in forward Na+/Ca2+ exchange activity provides a hypothetical explanation for the late action potential prolongation observed in this study.

Electrophysiological observations on diaphragm muscle from normal and dystrophic hamsters

1985 ◽  
Vol 63 (11) ◽  
pp. 1474-1476 ◽  
Author(s):  
E. G. Hunter ◽  
J. Elbrink
Keyword(s):  
Membrane Potential ◽  
Electrical Activity ◽  
Action Potentials ◽  
Membrane Potentials ◽  
Diaphragm Muscle ◽  
Resting Membrane Potential ◽  
Rapid Decline ◽  
Action Potential Amplitude ◽  
Dystrophic Muscle ◽  
Adenosine Triphosphate Production

The cellular electrical activity of diaphragm from F1B normal and BIO 14.6 dystrophic hamsters has been investigated using microelectrodes. Resting membrane potentials and action potentials were recorded from control muscles and from muscles exposed to 2,4-dinitrophenol. The action potentials of normal and dystrophic diaphragms were similar in amplitude and configuration. Treatment with 2,4-dinitrophenol caused the action potential amplitude of both diaphragms to decline by similar amounts. The control resting membrane potential of diaphragm from dystrophic hamsters is not significantly different from that of normal hamsters. Treatment with 2,4-dinitrophenol caused a linear decrease in the resting membrane potentials of both groups of muscles. Dystrophic muscle, however, showed a more rapid decline in excitability when exposed to 2,4-dinitrophenol. This suggests that adenosine triphosphate production in dystrophic muscle is partially inhibited as has been suggested by other workers.

scholarly journals Silica nanoparticles induce cardiotoxicity interfering with energetic status and Ca2+ handling in adult rat cardiomyocytes

2017 ◽  
Vol 312 (4) ◽  
pp. H645-H661 ◽  
Author(s):  
Carlos Enrique Guerrero-Beltrán ◽  
Judith Bernal-Ramírez ◽  
Omar Lozano ◽  
Yuriana Oropeza-Almazán ◽  
Elena Cristina Castillo ◽  
...  
Keyword(s):  
Silica Nanoparticles ◽  
Glutathione Depletion ◽  
Energy Status ◽  
Adrenergic Stimulation ◽  
Rat Cardiomyocytes ◽  
Atp Production ◽  
Adult Rat ◽  
Intracellular Ca ◽  
Rat Myocytes ◽  
Potential Risks

Recent evidence has shown that nanoparticles that have been used to improve or create new functional properties for common products may pose potential risks to human health. Silicon dioxide (SiO2) has emerged as a promising therapy vector for the heart. However, its potential toxicity and mechanisms of damage remain poorly understood. This study provides the first exploration of SiO2-induced toxicity in cultured cardiomyocytes exposed to 7- or 670-nm SiO2 particles. We evaluated the mechanism of cell death in isolated adult cardiomyocytes exposed to 24-h incubation. The SiO2 cell membrane association and internalization were analyzed. SiO2 showed a dose-dependent cytotoxic effect with a half-maximal inhibitory concentration for the 7 nm (99.5 ± 12.4 µg/ml) and 670 nm (>1,500 µg/ml) particles, which indicates size-dependent toxicity. We evaluated cardiomyocyte shortening and intracellular Ca2+ handling, which showed impaired contractility and intracellular Ca2+ transient amplitude during β-adrenergic stimulation in SiO2 treatment. The time to 50% Ca2+ decay increased 39%, and the Ca2+ spark frequency and amplitude decreased by 35 and 21%, respectively, which suggest a reduction in sarcoplasmic reticulum Ca2+-ATPase (SERCA) activity. Moreover, SiO2 treatment depolarized the mitochondrial membrane potential and decreased ATP production by 55%. Notable glutathione depletion and H2O2 generation were also observed. These data indicate that SiO2 increases oxidative stress, which leads to mitochondrial dysfunction and low energy status; these underlie reduced SERCA activity, shortened Ca2+ release, and reduced cell shortening. This mechanism of SiO2 cardiotoxicity potentially plays an important role in the pathophysiology mechanism of heart failure, arrhythmias, and sudden death. NEW & NOTEWORTHY Silica particles are used as novel nanotechnology-based vehicles for diagnostics and therapeutics for the heart. However, their potential hazardous effects remain unknown. Here, the cardiotoxicity of silica nanoparticles in rat myocytes has been described for the first time, showing an impairment of mitochondrial function that interfered directly with Ca2+ handling.

Physiological properties of primate lumbar motoneurons

1992 ◽  
Vol 68 (4) ◽  
pp. 1121-1132 ◽  
Author(s):  
J. S. Carp
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Cell Size ◽  
Current Pulse ◽  
Time Course ◽  
Triceps Surae ◽  
Resting Membrane Potential ◽  
Action Potential Amplitude ◽  
Lateral Gastrocnemius ◽  
Potential Amplitude

1. Intracellular recordings were obtained from 149 motoneurons innervating triceps surae (n = 109) and more distal muscles (n = 40) in 14 pentobarbital-anesthetized monkeys (Macaca nemestrina). The variables evaluated were resting membrane potential, action potential amplitude, conduction velocity (CV), input resistance (RN), membrane time constant (tau m), electrotonic length (L), whole-cell capacitance (Ctot), long current pulse threshold (rheobase), short current pulse threshold (Ishort), afterhyperpolarization (AHP) maximum amplitude (AHPmax), AHP duration (AHPdur), time to half maximum AHP amplitude (AHP t1/2), depolarization from resting potential to elicit action potential (Vdep), and threshold voltage for action potential discharge (Vthr). 2. Mean values +/- SD for the entire sample of motoneurons are as follows: resting membrane potential -67 +/- 6 mV; action potential amplitude 75 +/- 7 mV; CV 71 +/- 6 m/s; RN 1.0 +/- 0.5 M omega; tau m 4.4 +/- 1.5 ms; L 1.4 +/- 0.2 lambda; Ctot 7.1 +/- 1.8 nF; rheobase 13 +/- 7 nA; Ishort 29 +/- 14 nA; AHPmax 3.5 +/- 1.3 mV; AHPdur 77 +/- 26 ms; AHP t 1/2 21 +/- 7 ms; Vdep 11 +/- 4 mV; and Vthr -56 +/- 5 mV. CV is lower in soleus than in either medial or lateral gastrocnemius motoneurons, and RN is lower and tau m is longer in soleus than in lateral gastrocnemius motoneurons. 3. RN is higher in motoneurons with longer tau m and slower CV. A linear relationship exists between log(CV) and log(1/RN) with a slope of 1.8-2.2 (depending on the action potential amplitude acceptance criteria used), suggesting that membrane resistivity (Rm) does not vary systematically with cell size. 4. Rheobase is higher in motoneurons with lower RN, longer tau m, shorter AHP time course, and higher CV. Ishort and normalized rheobase (i.e., rheobase/Ctot) vary similarly with these motoneuron properties, except that Ishort is independent of tau m and normalized rheobase is independent of CV. 5. Vthr tends to be more depolarized in motoneurons with large Ctot, but the relationship is sufficiently weak so that any systematic variation in Vthr according to cell size probably contributes only minimally to recruitment order. Vthr does not vary systematically with CV, AHP time course, RN, or tau m. 6. Quantitative differences between macaque and cat triceps surae motoneurons are apparent in CV, which is slower in macaque than in cat, and to a lesser extent in tau m and RN, which are lower in macaque than in cat.(ABSTRACT TRUNCATED AT 400 WORDS)

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