• Journal of the korean academy of Pediatric Dentistry
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• v.27 no.3
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• pp.400-409
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• 2000

This study used in vivo intracellular and extracellular field potential recording to evaluate the intrinsic membrane properties and connection pattern within facial nucleus. 1. There were four subdivisions of medial, intermediate, lateral, and dorsolateral in facial nucleus. 2. Principal cells in the facial nucleus was recorded from and filled with neurobiotin in anesthetized rats. The extent of their dendrites and the characteristics of cell body were examined. 3. Principal cells had a large amplitude action potential and afterhyperpolarization was followed a single action potential. 4. The response from facial motonucleus to electrical stimulation of the facial nerve was mainly a monophasic wave, with a latency of 1 msec, which was assumed to reflect antidromic activation of facial motoneurons. In some of rats the response in addition showed late components at a latency of about 7-8 msec, but its amplitude was small. 5 Most of cells exhibited accommodation of spike discharge upon depolarization of membrane by 0.8 nA for 400 ms. Our results support the hypothesis that there normally are weak connections between different parts of the facial motonucleus to explain pathophysiology of hemifacial spasm and facial naive paralysis.

• The Journal of Korean Physical Therapy
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• v.14 no.2
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• pp.1-15
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• 2002

Excitation-contraction coupling in skeletal muscle is process by which depolarization of the muscle fiber membrane, elicited by a nerve action potential, triggers the release of $Ca^{2+}$ from the sarcoplasmic reticulum(SR). The resulting rise in intracellular $Ca^{2+}$ concentration$([Ca^{2+}]_i)$ activates the troponin complex, thereby initiating the contraction of the muscle. The question remains as to what factors are involved in the inhibition of SR $Ca^{2+}$ release in fatigued muscle. The purpose of this study was determine whether ATP-sensitive $K^+(K_{ATP})$ channels are activated and contribute to decrease in $[Ca^{2+}]_i$ during fatigue development in the mouse skeletal muscle. To elucidate a role of $K_{ATP})$ in relation to ECC, I measured the modulation effects of $K_{ATP})$ channel blocker(glibenclamide) and opener(pinacidil) on $[Ca^{2+}]_i$ after fatiguing electrical field stimulation(FEFS). Intracellular $Ca^{2+}$ signals were recorded by conforcal laser microscopy(LSM 410) and monitored using the fluorescent $Ca^{2+}$-Sensitive indicator Fluo-3 AM. The results of this study were as followed: 1. The relative [Ca2'li after FEFS in the pre-glibenclamide-treated group was higher than the control. And relative $[Ca^{2+}]_i$ after FEFS in the pre-glibenclamide-treated group was lower than the control. 2. The relative $[Ca^{2+}]_i$ after FEFS for 3 min in the control, pre-glibenclamide-treated group and pre-pinacidil-treated group showed a similar pattern; the gradually significant decrease in $[Ca^{2+}]_i$. But, these decreasing pattern was most significant in the control. These findings suggest a tight relationship between $K_{ATP})$ and $Ca^{2+}$ in ECC during fatigue. Therefore, 1 thought that activation of $K_{ATP})$ channels may be one of mechanisms of the fatigue in skeletal muscle.

• Korean Journal of Veterinary Research
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• v.35 no.3
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• pp.447-458
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• 1995

This study was carried out to characterize nonadrenergic, noncholinergic(NANC) relaxation of porcine retractor penis(PRP) muscle induced by electrical field stimulation(EFS) and to investigate the actions of niric oxide(NO) and vasoactive intestinal polypeptide(VIP) as candidates for NANC neurotransmitters. Biphasic relaxations of PRP muscle were induced by EFS to NANC nerve. Rapid-phase relaxation was observed at low frequency(0.5-16Hz) and slow-phase relaxation followed during high frequency(8-60Hz). Both relaxations were frequency-dependent and TTX($1{\times}10^{-6}M$)-sensitive. L-NAME($2{\times}10^{-5}M$) inhibited the rapid-phase relaxation, but not the slow-phase relaxation. The inhibition of the rapid-phase relaxation with L-NAME was reversed by L-arginine ($1{\times}10^{-3}M$) but not by D-arginine($1{\times}10^{-3}M$). Methylene blue($4{\times}10^{-5}M$) reduced the rapid-phase relaxation. Exogenous No(ExoNO, $1{\times}10^{-5}-1{\times}10^{-4}M$) induced dose-dependent relaxations of PRP muscle. Oxyhemoglobin($5{\times}1^{-5}M$) blocked the relaxation induced by ExoNO and inhibited EFS-induced relaxation. Hydroquinone($1{\times}10^{-4}M$) also abolished the relaxation induced by ExoNO, but did not affect EFS-induced relaxation. L-NAME resistant slow-phase relaxation to EFS was inhibited by ${\alpha}$-chymotrypsin(2.5 U/ml). Both methylene blue($4{\times}10^{-5}M$) and Nethylmaleimide($1{\times}10^{-4}M$) reduced the slow-phase relaxation by EFS. [4-Cl-D-$Phe^6$, $Leu^{17}$]-VIP($3{\times}10^{-6}M$) inhibited the slow-phase relaxation by EFS. External applications of VIP ($1{\times}10^{-7}M$) caused relaxations that were simillar to the L-NAME resistant slow-phase relaxations induced by EFS, and relaxant effects of exogenous VIP were blocked by ${\alpha}$-chymotrypsin(2.5 U/ml).

• The Korean Journal of Pharmacology
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• v.14 no.1_2
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• pp.33-40
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• 1978

1) The authors studied the effect of increasing age on the contraction and relaxation mechanism in the ureteral smooth muscle of the guinea pig. 2) Two to three week old, three month old, and two to three year old guinea pig ureters were used and the consistent amplitude of contratile responses were induced by using train stimulation. 3) After mounting the specimens in Tyrode's solution containing 2.6mM $Ca^{++}$, the ureter was stimulated, of which amplitude was initial contraction and next continuously superfused with $Ca^{++}$-free Tyrod's solution. When the contractile response stopped by electrical field stimulation, the muscle specimens was superfused with Tyrode's solution 0.25mM $Ca^{++}$ for 15min and stimulated with the same parameters. Thereafter, the contraction of $Ca^{++}$ in the solution was increased step by step up to 2.7mM. 4) The ureters of 2-3 week old guinea pigs needed less $Ca^{++}$ for the recovery of contractile response than those of three month and two to three year old did. In 2.7mM $Ca^{++}$, the ureters of 2-3 week and 3 month old guinea pigs recovered the contractile response of over 90% but those of 2-3 year old recovered the contractility of 77.2%. 5) Isoproterenol inhibited in dose dependent manner from $10^{-7}$ to $10^{-5}\;M$ ureteral contractility of both 2-3 week and 2-3 year old guinea pigs. The inhibition of the old ureter by isoproterenol was significantly less (P<0.025) than that of the younger ureter. However theophylline showed the strong inhibition independent of the function of age. 6) Dibutyryl cyclic AMP showed dose-dependent inhibition of the contraction of ureters of 2-3 week old guinea pigs but there was shown no inhibition in the old ureters. Further, the content of endogenous cyclic AMP in the two week old ureter was higher by 73% than that of 17 month old ureter. Cyclic GMP contents was not much different between two groups. 7) The ureteral smooth muscle of the younger guinea pig had more efficiency than that of the older animals in the mobilization and storage of calcium which concerned itself in the contraction and relaxation mechanism.

• Korean Journal of Animal Reproduction
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• v.24 no.4
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• pp.407-417
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• 2000

The present study was to examine effects of various electrical stimulus treatments used for electro-fusion on the preimplantation development of bovine nuclear transfer (NT) embryos with fetal fibroblast cells. Fetal fibroblast cells were isolated from one fetus at day 45 of gestation in Holstein cow, and passaged 3 to 4 times before being transferred into enucleated oocytes. Single fibroblast cells were individually placed into the perivitelline space of enucleated oocytes by using a micromanipulator. At first, the fusion and developmental rates of reconstructed oocytes were compared between different electric stimulation conditions. When fusion of the reconstructed oocyte was induced by different electric pulse periods (15, 30 and 45 $\mu$sec) at a DC pulse of 1.8 kV/cm, 15 (45.5%, 120/264) or 30 $\mu$ sec group (43.9%, 106/241) showed a higher fusion rate than 45 $\mu$sec group (23.2%, 58/250, P＜0.05). However, no difference was detected in the development rate of the fused oocytes to blastocysts between groups. Next experiment was to examine the effects of different electrical field strengths (1.5, 1.8 and 2.1 kV/cm) for 15 $\mu$sec at electrofusion on in vitro development of the NT embryos. As results, there was no difference in the fusion and developmental rates of the NT embryos between electrical strength (P＞0.05). Finally, developmental competence of bovine NT embryos with somatic cells was compared with IVF-derived embryos. Of enucleated oocytes fused with fibroblast cells, 27.4% (75/274) developed to the blastocyst stage, which is similar to that (24.5%, 58/237) of IVF-derived embryos. However, mean nuclei number of NT blastocysts was smaller than that of IVF-derived blastocysts. Thus, we have established an optimal condition (1.8 kV/cm, 15 $\mu$sec) for electric fusion of bovine NT oocytes with somatic cells. The present study indicates that bovine reconstructed embryos with somatic cells normally develop to blastocyst stage in vitro, although having smaller nuclei numbers of blastocysts as compared to IVF-derived embryos.

• Journal of Chest Surgery
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• v.23 no.3
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• pp.452-464
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• 1990

It is well known that extracellular Calcium plays a very important role in several steps of smooth muscle excitability and contractility, and there have been many concerns about factors influencing the distribution of extracellular Ca++ and the Ca++ flux through the cell membrane of the smooth muscle. Based on the assumption that Mg++ may also play an important role in the excitation and contraction processes of the smooth muscle by taking part in affecting Ca++ distribution and flux, many researches are being performed about the exact role of Mg++, especially in the vascular smooth muscle. But yet the effect of Mg++ in the smooth muscle activity is not clarified, and moreover the mechanism of Mg++ action is almost completely unknown. Present study attempted to clarify the effect of Mg++ on the excitability and contractility in the multiunit and unitary smooth muscle, and the mechanism concerned in it. The preparations used were the guinea-pig aortic strip as the experimental material of the multiunit smooth muscle and the rat uterine strip as the one of the unitary smooth muscle. The tissues were isolated from the sacrificed animal and were prepared for recording the isometric contraction. The effects of Mg++ and Ca++ were examined on the electrically driven or spontaneous contraction of the preparations. And the effects of these ions were also studied on the K+ or norepinephrine contracture. All experiments were performed in tris-buffered Tyrode solution which was aerated with 100% 02 and kept at 35oC. The results obtained were as follows: 1] Mg++ suppressed the phasic contraction induced by electrical field stimulation dose-dependently in the guinea-pig aortic strip, while the high concentration of Ca++ never recovered the decreased tension. These phenomena were not changed by the a - or b - adrenergic blocker. 2]Mg++ played the suppressing effect on the low concentration [20 and 40 mM] of K+-contracture in the aortic muscle, but the effect was not shown in the case of 100mM K+-contracture. 3] Mg++ also suppressed the contracture induced by norepinephrine in the aortic preparation. And the effect of Mg++ was most prominent in the contracture by the lowest [10 mM] concentration of norepinephrine. 4] In both the spontaneous and electrically driven contractions of the uterine strip, Mg++ decreased the amplitude of peak tension, and by the high concentration of Ca++ the amplitude of tension was recovered unlike the aortic muscle. 5] The frequency of the uterine spontaneous contraction increased as the [Ca++] / [Mg++] ratio increased up to 2, but the frequency decreased above this level. 6] Mg++ decreased the tension of the low[20 and 40mM] K+-contracture in the uterine smooth muscle, but the effect did not appear in the 100mM K+-contracture. From the above results, the following conclusion could be made. 1] Mg++ seems to suppress the contractility directly by acting on the smooth muscle itself, besides through the indirect action on the nerve terminal, in both the aortic and uterine smooth muscles. 2] The fact that the depressant effect of Mg++ on the K+-contracture is in inverse proportion to an increase of K+ concentration appears resulted from the extent of the opening state of the Ca++ channel. 3] Mg++ may play a depressant role on both the potential dependent and the receptor-operated Ca++ channels. 4] The relationship between the actions of Mg++ and Ca++ seems to be competitive in uterine muscle and non-competitive in aortic strip.