scholarly journals Effect of External Calcium and of Temperature on Contraction in Snake Muscle Fibers

1974 ◽  
Vol 63 (4) ◽  
pp. 415-431 ◽  
Author(s):  
Hiroshi Washio
Keyword(s):  
Time Course ◽  
Contractile Response ◽  
Muscle Fibers ◽  
Outward Current ◽  
Bathing Solution ◽  
Minimum Duration ◽  
Delayed Rectification ◽  
Rate Of Recovery ◽  
Lower Temperature ◽  
External Calcium

The effect of external calcium and of temperature on the contractile responses has been studied in voltage clamped snake twitch muscle fibers. Increasing [Ca++]o from 0.2 to 7.0 mM raised contractile threshold by 15–20 mV, the latter coinciding with the appearance of delayed rectification. The duration of contracture, the rates of rise and decay of tension depended on the level of depolarization and [Ca++]o. The minimum duration of repolarization necessary to restore the contractile response was much shorter in high [Ca++]o. When the bathing solution was cooled to 10 from 20°C the time-course of contracture was markedly prolonged and the outward current was reduced without significant change in maximum tension. The threshold for contraction tended to be somewhat lower at the lower temperature. The contractile repriming was much slower at low temperature. However, reduction in temperature slowed the rate of recovery much less at low [Ca++]o than at normal [Ca++]o.

scholarly journals The Effect of Glycerol Treatment of Voltage-Clamped Snake Muscle Fibers

1973 ◽  
Vol 61 (2) ◽  
pp. 176-184 ◽  
Author(s):  
Hiroshi Washio
Keyword(s):  
Normal Saline ◽  
Surface Membrane ◽  
Muscle Fibers ◽  
Outward Current ◽  
Tension Development ◽  
Normal Medium ◽  
Outward Currents ◽  
Delayed Rectification ◽  
Glycerol Treatment ◽  
Contractile Activation

The effect of glycerol treatment on the membrane currents and tension development was studied in voltage clamped snake muscle fibers. In muscle fibers which were exposed for 1 h to a normal saline containing 400 mM glycerol and then returned to a normal medium, graded depolarizations did not accompany contractile responses. However, when the fiber was depolarized to a certain level, an increment of outward current appeared which partially inactivated with time. The threshold for delayed rectification in glycerol-treated fibers was almost the same as that of intact fibers in spite of the absence of contractile tension. The results suggest that the delayed rectification may be attributed at least in part to the surface membrane and that the contractile activation probably does not depend simply on the inactivating outward currents through the delayed rectification channel.

Calcium and Contraction in the Rabbit Anterior Mesenteric–Portal Vein

1972 ◽  
Vol 50 (4) ◽  
pp. 289-299 ◽  
Author(s):  
G. A. Collins ◽  
M. C. Sutter ◽  
J. C. Teiser
Keyword(s):  
Portal Vein ◽  
Membrane Permeability ◽  
Time Course ◽  
Contractile Response ◽  
Calcium Influx ◽  
Contractile Activity ◽  
Krebs Solution ◽  
Free Solution ◽  
Membrane Bound ◽  
External Calcium

Studies were done measuring contractile activity in the isolated rabbit anterior mesenteric–portal vein (A.M.V.). The rabbit A.M.V. requires external calcium for both spontaneous activity and the initiation and maintenance of contractions to agonists.After bathing the tissues in calcium-free Krebs' solution containing 1 mM ethyleneglycoltetraacetic acid (EGTA) for 10 min, and then washing out the EGTA, the re-addition of calcium produced a contraction. The pre-addition of a small amount of calcium (0.1 mM) after EGTA treatment (while not inducing a contractile response) alters subsequent contractile responses to larger concentrations of calcium. This is interpreted as the ability of membrane-bound calcium to control membrane permeability to calcium.Other experiments involved bathing the tissues in calcium-free solution until no response was obtained to agonists, and then re-adding calcium. The time course of the responses to noradrenaline after calcium re-addition depended on the length of calcium incubation. This suggests that noradrenaline can release a loosely bound calcium fraction which may be involved in controlling calcium influx. This bound calcium, however, does not provide a major source of activator calcium in normal Krebs' solution.

scholarly journals Pseudo-streaming potentials in Necturus gallbladder epithelium. II. The mechanism is a junctional diffusion potential.

1992 ◽  
Vol 99 (3) ◽  
pp. 317-338 ◽  
Author(s):  
L Reuss ◽  
B Simon ◽  
C U Cotton
Keyword(s):  
Time Course ◽  
Bathing Solution ◽  
Intercellular Spaces ◽  
Similar Time ◽  
Streaming Potentials ◽  
Osmotic Water ◽  
Lateral Intercellular Spaces ◽  
Transepithelial Voltage ◽  
Time Courses ◽  
Good Agreement

The mechanisms of apparent streaming potentials elicited across Necturus gallbladder epithelium by addition or removal of sucrose from the apical bathing solution were studied by assessing the time courses of: (a) the change in transepithelial voltage (Vms). (b) the change in osmolality at the cell surface (estimated with a tetrabutylammonium [TBA+]-selective microelectrode, using TBA+ as a tracer for sucrose), and (c) the change in cell impermeant solute concentration ([TMA+]i, measured with an intracellular double-barrel TMA(+)-selective microelectrode after loading the cells with TMA+ by transient permeabilization with nystatin). For both sucrose addition and removal, the time courses of Vms were the same as the time courses of the voltage signals produced by [TMA+]i, while the time courses of the voltage signals produced by [TBA+]o were much faster. These results suggest that the apparent streaming potentials are caused by changes of [NaCl] in the lateral intercellular spaces, whose time course reflects the changes in cell water volume (and osmolality) elicited by the alterations in apical solution osmolality. Changes in cell osmolality are slow relative to those of the apical solution osmolality, whereas lateral space osmolality follows cell osmolality rapidly, due to the large surface area of lateral membranes and the small volume of the spaces. Analysis of a simple mathematical model of the epithelium yields an apical membrane Lp in good agreement with previous measurements and suggests that elevations of the apical solution osmolality elicit rapid reductions in junctional ionic selectivity, also in good agreement with experimental determinations. Elevations in apical solution [NaCl] cause biphasic transepithelial voltage changes: a rapid negative Vms change of similar time course to that of a Na+/TBA+ bi-ionic potential and a slow positive Vms change of similar time course to that of the sucrose-induced apparent streaming potential. We conclude that the Vms changes elicited by addition of impermeant solute to the apical bathing solution are pseudo-streaming potentials, i.e., junctional diffusion potentials caused by salt concentration changes in the lateral intercellular spaces secondary to osmotic water flow from the cells to the apical bathing solution and from the lateral intercellular spaces to the cells. Our results do not support the notion of junctional solute-solvent coupling during transepithelial osmotic water flow.

scholarly journals Charge Movement Associated with the Opening and Closing of the Activation Gates of the Na Channels

1974 ◽  
Vol 63 (5) ◽  
pp. 533-552 ◽  
Author(s):  
Clay M. Armstrong ◽  
Francisco Bezanilla
Keyword(s):  
Time Course ◽  
Sodium Current ◽  
Close Association ◽  
Outward Current ◽  
Transient Outward Current ◽  
Activation Process ◽  
Charge Movement ◽  
Gating Current ◽  
Dipolar Molecules ◽  
Opening And Closing

The sodium current (INa) that develops after step depolarization of a voltage clamped squid axon is preceded by a transient outward current that is closely associated with the opening of the activation gates of the Na pores. This "gating current" is best seen when permeant ions (Na and K) are replaced by relatively impermeant ones, and when the linear portion of capacitative current is eliminated by adding current from positive steps to that from exactly equal negative ones. During opening of the Na pores gating current is outward, and as the pores close there is an inward tail of current that decays with approximately the same time-course as INa recorded in Na-containing medium. Both outward and inward gating current are unaffected by tetrodotoxin (TTX). Gating current is capacitative in origin, the result of relatively slow reorientation of charged or dipolar molecules in a suddenly altered membrane field. Close association with the Na activation process is clear from the time-course of gating current, and from the fact that three procedures that reversibly block INa also block gating current: internal perfusion with Zn2+, prolonged depolarization of the membrane, and inactivation of INa with a short positive prepulse.

scholarly journals Evaluation of Cardiovascular Experiment Animal

2021 ◽  
Vol 9 (12) ◽  
pp. 2305-2310
Author(s):  
Kirtane Ramesh Kirtane
Keyword(s):  
Myocardial Infarction ◽  
Coronary Artery ◽  
Time Course ◽  
Muscle Fibers ◽  
Early Mortality ◽  
Ground Substance ◽  
Coronary Artery Ligation ◽  
Time Intervals ◽  
In Vivo Models ◽  
Immunohistochemical Studies

Abstract: In vivo models of myocardial infarction induced by coronary artery ligation in rats usually suffer from high early mortality and a low rate of induction. This study investigated the time course initiation of chronic myocardial infarction in albino rats and the possibility of reducing early mortality rate due to myocardial infarction by modification of the surgical technique. CAL was carried out by passing the suture through the pericardial layer around the midway of the left anterior descending coronary artery including a small area of the myocardium to avoid mechanical damage to the heart geometry. In addition, the role of endothelin-1 in rat heart with congestive heart failure was critically assessed. Time course initiation experiments were designed by sacrificing the animals at different time intervals and by carrying out physiological, biochemical, histopathological, electron microscopical and immunohistochemical studies. Specific markers of myocardial injury, viz. cardiac troponin-T, high sensitivity C-reactive protein, lactate dehydrogenase and fibrinogen were measured at different time points. Serum marker enzymes and activities of lysosomal hydrolases were found to be elevated on the eighth day post-ligation. Histopathological studies demonstrated focal areas showing fibrovascular tissue containing fibroblasts, collagenous ground substance and numerous small capillaries replacing cardiac muscle fibers. Transmission electron micrographs exhibited mitochondrial changes of well-developed irreversible cardiac injury, viz. swelling, disorganization of cristae, appearance of mitochondrial amorphous matrix densities, and significant distortion of muscle fibers and distinct disruption of the intercalated discs. Immune blotting studies confirmed the presence of alpha 2-macroglobulin which supported the inflammatory response. The severity of the CMI was inferred by the measurement of the level of ET-1 in plasma and left ventricle which was significantly higher in the CMI rats than in the sham-operated rats. Immunohistochemical studies at different time intervals showed that there was a significant immunoexpression of ET-1 on the eighth day post-ligation. This study conclusively showed that ligation of left anterior descending artery minimised mortality and ET-1 was expressed during CMI.

Long-lasting reduction of excitability by a sodium-dependent potassium current in cat neocortical neurons

1989 ◽  
Vol 61 (2) ◽  
pp. 233-244 ◽  
Author(s):  
P. C. Schwindt ◽  
W. J. Spain ◽  
W. E. Crill
Keyword(s):  
Voltage Clamp ◽  
Time Course ◽  
Outward Current ◽  
Repetitive Firing ◽  
K Channel ◽  
Channel Blockers ◽  
Dantrolene Sodium ◽  
Current Time ◽  
Tail Current ◽  
Neocortical Neurons

1. The function and ionic mechanism of a slow outward current were studied in large layer V neurons of cat sensorimotor cortex using an in vitro slice preparation and single microelectrode voltage clamp. 2. With Ca2+ influx blocked, a slow relaxation ("tail") of outward current followed either (1) repetitive firing evoked for 1 s or (2) a small 1-s depolarizing voltage clamp step that activated the persistent Na+ current of neocortical neurons, INaP. When a depolarization that activated INaP was maintained, an outward current gradually developed and increased in amplitude over a period of tens of seconds to several minutes. An outward tail current of similar duration followed repolarization. The slow outward current was abolished by TTX, indicating it depended on Na+ influx. 3. With Ca2+ influx blocked, the onset of the slow Na+-dependent outward current caused spike frequency adaptation during current-evoked repetitive firing. Following the firing, the decay of the Na+-dependent current caused a slow afterhyperpolarization (sAHP) and a long-lasting reduction of excitability. It also was responsible for habituation of the response to repeated identical current pulses. 4. The Na+-dependent tail current had properties expected of a K+ current. Membrane chord conductance increased during the tail, and tail amplitude was reduced or reversed by membrane potential hyperpolarization and raised extracellular K+ concentration [( K+]0). 5. The current tail was reduced reversibly by the K+ channel blockers TEA (5-10 mM), muscarine (5-20 microM), and norepinephrine (100 microM). These agents also resulted in a larger, more sustained inward current during the preceding step depolarization. Comparison of current time course before and after the application of blocking agents suggested that, in spite of its capability for slow buildup and decay, the onset of the Na+-dependent outward current occurs within 100 ms of an adequate step depolarization. 6. With Ca2+ influx blocked, extracellular application of dantrolene sodium (30 microM) had no clear effect on the current tail or the corresponding sAHP.(ABSTRACT TRUNCATED AT 400 WORDS)

A Calcium-Dependent Mechanism Responsible for Increasing the Freezing Tolerance of the Bivalve Mollusc Modiolus Demissus

1977 ◽  
Vol 69 (1) ◽  
pp. 13-21
Author(s):  
DENNIS J. MURPHY
Keyword(s):  
Low Temperature ◽  
Freezing Tolerance ◽  
Time Course ◽  
Cell Membranes ◽  
Contractile Response ◽  
Temperature Acclimation ◽  
Freezing Injury ◽  
Total Change ◽  
Calcium Dependent ◽  
Dependent Mechanism

1. A time course of the changes in blood Ca2+ and freezing tolerance of Modiolus demissus (Dillwyn) demonstrated that increases in freezing tolerance parallel increases in blood Ca2+. The increases in freezing tolerance occurred rapidly, suggesting that Ca2+ affects freezing tolerance directly by its presence in the blood. 2. The presence of La3+ reduced the freezing tolerance of isolated foot muscle. Thus, Ca2+ appears to increase freezing tolerance directly by binding to cell membranes. 3. The loss of the contractile response of freeze-thawed foot muscle to Ach, KCl and caffeine and the continued response to CaCl2 suggested that cell membranes are the primary sites of freezing injury. 4. The increase in blood Ca2+ following low-temperature acclimation accounted for only 40% of the total change in freezing tolerance. Therefore, other mechanisms responsible for increasing the freezing tolerance of M. demissus following low temperature acclimation also exist.

The Effect of Changed Extracellular Calcium and Sodium Concentration on the Electroretinogram of the Crayfish Retina

1980 ◽  
Vol 35 (3-4) ◽  
pp. 308-318 ◽  
Author(s):  
H. Stieve ◽  
I. Claßen-Linke
Keyword(s):  
Dark Adaptation ◽  
Time Course ◽  
Calcium Concentration ◽  
Light Adaptation ◽  
Sodium Concentration ◽  
Strong Increase ◽  
Calcium Stores ◽  
Half Time ◽  
Astacus Leptodactylus ◽  
External Calcium

Abstract The electroretinogram (ERG) of the isolated retina of the crayfish Astacus leptodactylus evoked by strong 10 ms light flashes at constant 5 min intervals was measured while the retina was continuously superfused with various salines which differed in Ca2+ -and Na+ -concentrations. The osmotic pressure of test- and reference-saline was adjusted to be identical by adding sucrose. Results: 1. Upon raising the calcium-concentration of the superfusate in the range of 20-150 mmol/l (constant Na+ -concentration: 208 mmol/l) the peak amplitude hmax and the half time of decay t2 of the ERG both decrease gradually up to about 50% in respect to the corresponding value in reference saline. 2. The recovery of the ERG due to dark adaptation following the “weakly light adapted state” is greatly diminished in high external [Ca2+]ex. 3. Lowering the external calcium-concentration (10 →1 mmol/l) causes a small increase in hmax and a strong increase of the half time of decay t2 (about 180%). Upon lowering the calcium concentration of the superfusate to about 1 nmol/l by 1 mmol/l of the calcium buffer EDTA, a slowly augmenting diminution of the ERG height hm SLX occurs. How­ever, a strong retardation of the falling phase of the ERG characterized by an increase in t2 occurs quickly. Even after 90 min stay in the low calcium saline the retina is still not inexcitable; hmax is 5 - 10% of the reference value. The diminution of hmax occurs about six-fold faster when the buffer concentration is raised to 10 mmol/l EDTA. 4. Additional lowering of the Na+ -concentration (208 →20.8 mmol/l) in a superfusate with a calcium concentration raised to 150 mmol/l causes a strong reduction of the ERG amplitude hmax to about 10%. 5. In a superfusate containing 1 nmol/l calcium such lowering of the sodium concentration (208 → 20.8 mmol/l) causes a diminution of the ERG height to about 40% and the shape of the ERG to become polyphasic; at least two maxima with different time to peak values are observed. Interpretation: 1. The similarity of effects, namely raising external calcium concentration and light adaptation on the one hand and lowering external calcium and dark adaptation on the other hand may indicate that the external calcium is acting on the adaptation mechanism of the photoreceptor cells, presumably by influencing the intracellular [Ca2+]. 2. The great tolerance of the retina against Ca2+ -deficiency in the superfusate might be effected by calcium stores in the retina which need high Ca2+ -buffer concentrations in the superfusate to become exhausted. 3. In contrast to the Limulus ventral nerve photoreceptor there does not seem to be an antagonis­ tic effect of sodium and calcium in the crayfish retina on the control of the light channels. 4. The crayfish receptor potential seems to be composed of at least two different processes. Lowering calcium-and lowering external sodium-concentration both diminish the height and change the time course of the two components to a different degree. This could be caused by in­ fluencing the state of adaptation and thereby making the two maxima separately visible.

Time course of postnatal changes in rat heart action potential and in transient outward current is different

1994 ◽  
Vol 267 (3) ◽  
pp. H1157-H1166 ◽  
Author(s):  
G. M. Wahler ◽  
S. J. Dollinger ◽  
J. M. Smith ◽  
K. L. Flemal
Keyword(s):  
Action Potential ◽  
Rat Heart ◽  
Action Potentials ◽  
Time Course ◽  
Outward Current ◽  
Transient Outward Current ◽  
Papillary Muscles ◽  
Isolated Cells ◽  
Time Courses ◽  
Action Potential Shortening

The rat ventricular action potential shortens after birth. The contribution of increases in the transient outward current (Ito) to postnatal action potential shortening was assessed by measuring Ito in isolated cells and by determining the effect of 2 mM 4-aminopyridine (4-AP) on the action potentials of papillary muscles. 4-AP had no effect on 1-day action potential duration at 25% repolarization (APD25), and 1-day cells had little Ito. In 8- to 10-day muscles, 4-AP caused a small, but significant, increase in APD25. Ito increased slightly between day 1 and days 8-10, but this increase was not significant. Most of the increase in Ito (79%) and in the response to 4-AP (64%) occurred between days 8-10 and adult; however, approximately 75% of the APD25 shortening took place by days 8-10. Thus, while Ito may contribute to repolarization in late neonatal and adult cells, the different time courses of action potential shortening and increases in Ito suggest that changes in Ito are unlikely to be responsible for most of the postnatal action potential shortening.

Differential recovery of acetylcholinesterase in guinea pig muscle and brain regions after soman treatment

1998 ◽  
Vol 17 (3) ◽  
pp. 157-162 ◽  
Author(s):  
Maxine C Lintern ◽  
Janet R Wetherell ◽  
Margaret E Smith
Keyword(s):  
Enzyme Activity ◽  
Time Course ◽  
Brain Regions ◽  
Similar Rate ◽  
Molecular Forms ◽  
Similar Degree ◽  
Brain Areas ◽  
Pig Muscle ◽  
Rate Of Recovery ◽  
The Brain

1 In brain areas of untreated guinea-pigs the highest activity of acetylcholinesterase was seen in the striatum and cerebellum, followed by the midbrain, medulla-pons and cortex, and the lowest in the hippocampus. The activity in diaphragm was sevenfold lower than in the hippocampus. 2 At 1 h after soman (27 mg/kg) administration the activity of the enzyme was dramatically reduced in all tissues studied. In muscle the three major molecular forms (A12, G4 and G1) showed a similar degree of inhibition and a similar rate of recovery and the activity had returned to normal by 7 days. 3 In the brain soman inhibited the G4 form more than the G1 form. The hippocampus, cortex and midbrain showed the greatest reductions in enzyme activity. At 7 days the activity in the cortex, medulla pons and striatum had recovered but in the hippocampus, midbrain and cerebellum it was still inhibited. 4 Thus the effects of soman administration varied in severity and time course in the different tissues studied. However the enzyme activity was still reduced in all tissues at 24 h when the overt signs of poisoning had disappeared.

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