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Biomedical subjects

I Kosaka

Publications and source records attributed to I Kosaka.

11 recordsLinked to original sources

Reappraisal of projection levels of the corticospinal fibers in the cat, with special reference to the fibers descending through the dorsal funiculus: a WGA-HRP study.

The precise course and termination levels of the corticospinal tract (CST) in the cat were studied using the anterograde transport of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP). Following injection of WGA-HRP into the pericruciate (sensorimotor) cortex on one side, we observed the precise caudal termination levels of the CST fibers in the lateral and ventral funiculi. Simultaneously, the bilateral CSTs descending through the dorsal funiculus of the spinal cord were identified. Anterogradely labeled CST fibers within the lateral and ventral funiculi were observed bilaterally to reach the level of the third sacral (S3) spinal segment, which is lower than that ever described. The lowest level of the CST fibers within the dorsal funiculus, however, reached the level of the first sacral (S1) spinal segment. In conclusion, this study demonstrates that, in the cat, there exist 6 different CSTs (crossed and uncrossed lateral, ventral, dorsal) and that the termination levels of the lateral and ventral CSTs are much lower than those described in previous reports.

Animals↗

Anatomical evidence for the re-crossing of lateral corticospinal fibers via the posterior gray commissure in the cat spinal cord.

This study demonstrated the projections of the corticospinal tract (CST) by using the anterograde transport of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP). Following injection of WGA-HRP into the pre- and post-cruciate cortices (somatosensory area) on one side, labeled fibers were found in the spinal cord both in the lateral and in the anterior CSTs; both crossed, and uncrossed. The most conspicuous labeling was found in the crossed lateral CST. In addition, labeled lateral CST fibers were seen to recross via the posterior gray commissure. These re-crossed lateral CST fibers were most frequently observed in the cervical spinal segments.

Afferent Pathways↗

Carbachol contracture of stomach smooth muscle of the newt in calcium-free solution.

A small muscle preparation of stomach circular muscle of the newt responded to carbachol (CCh) with a phasic contracture. At 20 degrees C, in Ca-free Ringer solution (+1 mM EGTA), the amplitude of CCh contracture was very rapidly inhibited to less than 10% of that in normal Ringer solution (1.8 mM Ca). The amplitude of this CCh contracture was markedly enhanced with increasing [K]0. CCh contracture in Ca-free Ringer solution was also enhanced after K contracture was induced once in the presence of 1.8 mM Ca, followed by soaking in normal Ringer solution. The amplitude of this enhanced CCh contracture persisted up to about 5 min, following rapid decrease to about 70%, and then gradually decreased to a steady level in Ca-free Ringer solution. This decrease in amplitude was prevented by increasing [K]0 during soaking in Ca-free solution; even when the temperature was elevated from 20 to 35 degrees C during the periods of soaking in Ca-free solution, CCh contracture was inhibited only by about 20% in Ca-free high K solution, whereas in Ca-free or Ca-free low Na (Tris) Ringer solution it was inhibited by more than 50%.

Animals↗

Calcium loading properties of carbachol-sensitive calcium store in calcium-depleted stomach smooth muscle of the newt.

The amount of carbachol (CCh)-sensitive Ca store, which was loaded during Ca contracture in Ca-depleted stomach smooth muscle of the newt, was estimated from the amplitude of the CCh contracture induced in Ca-free high K solution. This store was loaded to nearly maximum level by simultaneous application of 2.8 X 10(-6)M Ca and 113.5 mM K, while Ca contracture induced at this time was less than 10% in amplitude of control (1.8 mM Ca). When the loading was interrupted after 5 sec of 1.8 mM Ca application, the amplitude of Ca contracture reached nearly its maximum, while the loading of the store was only about 30% of that after 90 sec. Contracture induced by Ca-free high K solution immediately after the brief (10 sec) exposure of the muscle to 1.8 mM Ca was about 50% that of K contracture, while little Ca was observed to be loaded. The [K]0-Ca contracture tension relation and the [K]0-Ca loading relation showed sigmoid and linear characteristics, respectively.

Animals↗

Contribution of intracellular stored calcium to contractile activation in contractures of stomach circular muscle of Bufo vulgaris formosus.

Contractile responses of stomach circular muscle of Bufo to high-K, to acetylcholine (ACh) in normal Ringer or in high-K solution, and to calcium in Ca-free high-K solution showed a phasic contraction which relaxed completely in 30-45 sec. K-induced contracture was abolished in Ca-free solution containing 1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) within 20 sec, while ACh-induced contracture was not abolished and 10-25% of control tension was kept up to 40 sec. This response increased to 40-50% when all extracellular Na was replaced with tris(hydroxymethyl)-aminomethane (Tris). K-induced contracture was inhibited completely by 1 mM La. ACh-induced contracture in the muscle depolarized by high-K solution was dependent on the depolarization time, 0-10, 60-70, and nearly 100% of control after 1, 3, and 10 min depolarization, respectively. These ACh-induced contractures were not inhibited by 1 mM EGTA or La. All contractures mentioned above were markedly inhibited by 5 mM procaine. These results suggest that activation of both contractures induced by high-K and ACh were, at least partly, dependent on the Ca at the intracellular Ca storage sites. Ca-induced contracture was dependent on depolarization time as was ACh-induced contracture, when the muscle was depolarized by Ca-free high-K solution without pre-treatment with Ca-free Ringer solution. These results suggest that activation of Ca-contracture is also dependent on intracellular stored Ca.

Acetylcholine↗

Potassium contracture in the tonic bundle isolated from the enlarged flexor carpi radialis muscle of the frog.

The flexor carpi radialis muscle (FCRM) of the frog was divided into phasic and tonic bundles, and the properties of the potassium contracture in the tonic bundle were examined. The potassium contracture was tonic and the contracture induced by K higher than 75 mM consisted of the initial phasic component and of the following sustained component. Both components were abolished by the transverse tubule disruption. The curve relating the peak tension to the log[K]o (activation curve) started at about 15 mM K and reached maximum at about 75 mM K. By reducing [Ca]o, the activation curve shifted downward at higher [K]o, being little affected near the mechanical threshold. The time course of inactivation induced by 20 mM K was slow and monophasic, and was markedly accelerated by reducing [Ca]o. The spontaneous relaxation of the contracture induced by high K was little affected by reducing [ca]o.

Animals↗

Biphasic time course of inactivation of potassium contractures in single twitch muscle fibers of the frog.

The time course of the inhibition of peak tension (inactivation) of potassium contracture induced by conditioning depolarization with 10, 15, 20 and 30 mM K+ was examined, using single twitch fibers from the frog semitendinosus muscle. The time-dependence curve of the inactivation was biphasic, consisting of the first phase and the second phase. The first phase was characterized as follows: 1) the time course and the extent depend on the degree of conditioning depolarization; 2) the inactivation proceeds exponentially and finally reaches a steady level; and 3) the rate is markedly increased by lowering Ca2+ in the external medium. It could be considered that the first phase of the inactivation is an analogical phenomenon with the inactivation of sodium conductance in a squid giant axon. The second phase of the inactivation induced by conditioning with 20 and 30 mM K+ reached its full inactivation independently of the degree of conditioning depolarization. On the basis of these results, the terms inactivation 1 and inactivation 2 were given to the first phase and second phase, respectively, of the time-dependence curve of the inactivation of potassium contracture.

Animals↗

Time- and Na-dependent effects of Ca depletion on potassium contracture in frog twitch muscle fiber.

The effect of the extracellular Ca depletion on potassium contracture was investigated in single fibers isolated from frog semitendinosus muscle mainly in relation to its time and Na dependency. The shortening of plateau duration and the increase in the rate of relaxation of the potassium contracture appeared within 3--5 sec and 15 sec, respectively, after the fiber was immersed in Ca-free Na Ringer solution containing 1 mM ethylene glycol bis(beta-aminoethyl ether)-N,N'-tetraacetic acid (EGTA) (EGTA-Na Ringer solution) or Ca-free choline Ringer solution containing 1 mM (EGTA (EGTA-choline Ringer solution). These effects were independent of the presence or absence of extracellular Na. In EGTA-Na Ringer solution, the potassium contracture tension was inhibited only by about 20% after 20--90 min and was abolished after 120 min. The inhibition of the peak tension was accelerated by the depletion of extracellular Na; in EGTA-choline Ringer solution, the tension was gradually inhibited by about 20% during the first 7 min and abolished after 10--12 min. When the peak tension of potassium contracture was abolished in EGTA-choline Ringer solution, the depolarization by Ca depletion was about 10 mV and the caffeine contracture was sufficiently produced. The results suggest that the inhibition of the potassium contracture tension in EGTA-choline Ringer solution is due to the dissociation of excitation-contraction coupling. On the basis of these results, an aspect of the inactivation of the potassium contracture was proposed.

Animals↗

Role of superficially membrane-bound calcium on excitation-contraction coupling in frog skeletal muscle.

Single fibers isolated from frog semitendinosus muscle continued to twitch for 5-8 min in calcium-free Ringer solution containing 1 mM ethylene glycol bis (beta-aminoethyl ether)-N, N'-tetraacetic acid (EGTA). Even after twitching was completely abolished, the tension of potassium contracture was not depressed, although the time course was markedly shortened. The resting potential recorded from single fibers 10 min after immersion in EGTA-Ringer solution decreased slightly. These fibers failed to generate action potential, however, in a whole sartorius muscle the self-exchangeable calcium was not significantly reduced by 1mM EGTA, while it was reduced by about 27% during the potassium contracture induced in the EGTA solution. From these results, it is suggested that the calcium bound on the surface sites of the transverse tubular membrane and the sarcolemma can serve as a trigger for the release of calcium from the sarcoplasmic reticulum and can produce a resting potential and maintain relatively long duration excitability under the condition of extracellular calcium deficiency.

Action Potentials↗