• Proceedings of the Korean Biophysical Society Conference
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• 1999.06a
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• pp.61-62
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• 1999

;The mechanisms inducing hypertension are actively investigated and are still challenging topics. Basically hypertension must be caused by the disorder of $Ca^{2+}$ metabolism in vascular smooth muscle, such as the increase of $Ca^{2+}$ influx, the decrease of ci+ efflux, or the change of sensitivity of contractile protein etc. The one of cause of the increase of ci+ influx may be the change of ci+ channel activity. Even though the relationships of ci+ channel activity and hypertension were studied using various hypertension models, still it is not clear how much change of $Ca^{2+}$ channel activity in diabetes mellitus (DM) induced hypertension is occurred. We induced DM hypertension in SD rat and compared the $Ca^{2+}$ channel activity with age-matched normotensive SD rat. For inducing DM hypertension, left kidney was removed with 200 gm rat and, after 1 month, 60 mg/kg of streptozotocin was injected into peritoneal space to induce diabetes mellitus. Usually after 4-6 weeks, hypertension was fully induced. For isolating vascular smooth muscle cells (VSMC), we used mesenteric arteriole (3rd - 4th branch of mesenteric artery) of which diameter is below 150 urn. VSMCs were isolated enzymatically. $Ca^{2+}$ current was measured using whole cell patch clamp technique. All experiments were performed at $37^{\circ}C$. The cell membrane area of VSMC of DM hypertensive rat is larger than that of control VSMC($36.6{\pm}3.64{\;}pF{\;}vs{\;}22.4{\pm}1.29{\;}pF, {\;}mean{\pm}S.E.$) When we compared the current amplitude, the $Ca^{2+}$ current amplitude in VSMC of DM hypertensive rat is much larger than that in VSMC of normotensive age-matched rat. After $Ca^{2+}$ current amplitude was normalized by cell membrane area, the current amplitude in DM hypertension is increased to $249.1{\pm}15.9{\;}%{\;}(mean{\pm}S.E.M)$, which means the ;absolute current amplitude is about 4 times larger in DM hypertension. When we compared the steady state activation and inactivation. there were no noticeable differences. From these results. one of cause of the DM hypertension is due to the increase of $Ca^{2+}$ current amplitude. But it need further study why the $Ca^{2+}$ current is so large in VSMC of DM hypertension and how much $Ca^{2+}$ influx through $Ca^{2+}$ channel contribute to the increase of intracellular $Ca^{2+}$ and eventually contribute to development of hypertension.ypertension.

• The Journal of the Korea Contents Association
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• v.9 no.9
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• pp.278-286
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• 2009

The aims of this study were to determined whether excitability of the $\alpha$-motor neuron is modulated by stretching and this changes were associated with flexibility of the muscle. In this study, $\alpha$-motor neuron excitability was measured by using the Hmax/Mmax ratio of the gastrocnemius H-reflex, and muscle flexibility was measured with the range of motion of the ankle dorsiflexion. The gastrocnemii of 10 healthy volunteers were stretched for 4 minutes(2 minutes stretching, 1 minute rest, and 2 minutes stretching) in each session by manual force. The Hmax/Mmax ratio of the H-reflex, as well as the range of motion of the ankle dosiflexion was measured through four different conditions: before stretching, as soon as after $1^{st}$ stretching, as soon as after $2^{nd}$ stretching and at 48 hours after $2^{nd}$ stretching. Excitability of the $\alpha$-motor neuron was decreased significantly after $1^{st}$ and $2^{nd}$ stretching(p<0.05). Furthermore, the range of the dorsiflexion was increased significantly after $1^{st}$ and $2^{nd}$ stretching(p<0.05). However, the excitability of the $\alpha$-motor neuron and range of the dorsiflexion at 48 hours after $2^{nd}$ stretching were not different from those of before stretching. These results suggest that reduced $\alpha$-motor neuron excitability of the gastrocnemius and increased flexibility of the ankle dorsiflexion would be followed by activation of the type III mechanoreceptor which around the ankle joint and the Golgi tendon organ in the gastrocnemius.

• Journal of the Korea Academia-Industrial cooperation Society
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• v.22 no.2
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• pp.659-666
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• 2021

This study aimed to investigate the effect of changes in pressure levels and gaze directions on deep neck flexor muscle thickness. Twenty-seven subjects participated in this study. Ultrasound imaging of the longus colli (LC) and sternocleidomastoid (SCM) were measured in four gaze directions (0°, 20°, 40°, 60°) and five pressure levels (20 mmHg, 22 mmHg, 24 mmHg, 26 mmHg, 28 mmHg) during cranial-cervical flexor (CCF) exercises. Repeated ANOVA was performed for analysis of muscle thickness difference according to gaze direction and pressure levels in LC and SCM. Results: LC showed a significant difference between 0° and 20°, 0° and 40°, and 0° and 60° at pressures of 20 mmHg and 22 mmHg (p<.05). SCM displayed a significant difference between 0° and 20°, 20° and 40°, and 40° and 60° at 28 mmHg (p<.05). In this study, it was found that setting the gaze direction to 20° for the CCF exercise can increase the activation of LC and lower the activity of SCM to obtain the effect of exercise. Based on the results of this study, it is hoped that the beneficial effects of the CCF exercise can be increased by setting an optimal gaze direction in a clinical environment.

• The Korean Journal of Physiology and Pharmacology
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• v.26 no.4
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• pp.277-285
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• 2022

To investigate the adverse effects of clozapine on cardiovascular ion channels, we examined the inhibitory effect of clozapine on voltage-dependent K⁺ (Kv) channels in rabbit coronary arterial smooth muscle cells. Clozapine-induced inhibition of Kv channels occurred in a concentration-dependent manner with an half-inhibitory concentration value of 7.84 ± 4.86 µM and a Hill coefficient of 0.47 ± 0.06. Clozapine did not shift the steady-state activation or inactivation curves, suggesting that it inhibited Kv channels regardless of gating properties. Application of train pulses (1 and 2 Hz) progressively augmented the clozapine-induced inhibition of Kv channels in the presence of the drug. Furthermore, the recovery time constant from inactivation was increased in the presence of clozapine, suggesting that clozapine-induced inhibition of Kv channels is use (state)-dependent. Pretreatment of a Kv1.5 subtype inhibitor decreased the Kv current amplitudes, but additional application of clozapine did not further inhibit the Kv current. Pretreatment with Kv2.1 or Kv7 subtype inhibitors partially blocked the inhibitory effect of clozapine. Based on these results, we conclude that clozapine inhibits arterial Kv channels in a concentration-and use (state)-dependent manner. Kv1.5 is the major subtype involved in clozapine-induced inhibition of Kv channels, and Kv2.1 and Kv7 subtypes are partially involved.

• Applied Microscopy
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• v.40 no.4
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• pp.261-266
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• 2010

ATP is the energy source synthesized at the electron transferase that consist of complex I, II, III, IV and V in mitochondrial cristae. The complex V functions as ATPase which composed of sub-complex $F_0$ and $F_1$. Porin or VDAC (voltagedependent anion-selective channel), is a family of small pore-forming proteins of the mitochondrial outer membrane, and play important roles in the regulated flux of anion, proton and metabolites between the cytosolic and mitochondrial compartments. The channel allows the diffusion of negatively charged solutes such as succinate, malate, and ATP in the fully open state, but of positively charged ions in subconducting state. In this study, in order to investigate the relationship of the function and localization between porin and ATPase we observed the distribution of porin and ATPase in the mitochondria of the bovine heart. Monoclonal antibodies against porin and ATPase ${\beta}$-subunit were used to detect porin and ATPase using light microscope with immunohistochemistry and immunofluorescence, and using electron microscope with immunogold-labeling. ATPase were stained in longitudinal section region in cardiac muscle, porin were stained in longitudinal section region in cardiac muscle. We viewed more specific pattern of localization and distribution of these proteins using immunofluorescence method. There were some region which were labeled with porin or ATPase respectively, and others which were labeled both proteins in cardiac muscle. The electron microscope results showed that immunogold labeled porin were labeled locally at mitochondrial outer membrane and ATPase were labeled evenly at mitochondrial cristae. But ATPase was not labeled at mitochondria cristae. These results confirmed the subcellular localizations of porin and ATPase in mitochondrial outer membrane and cristae. Also, we assumed that ATP synthesis always does not activation in all mitochondria exist in the bovine cardiac muscle.

• Sleep Medicine and Psychophysiology
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• v.5 no.2
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• pp.119-133
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• 1998

Attentional processes facilitate cognitive and behavioral performance in several ways. Attention serves to reduce the amount of information to receive. Attention enables humans to direct themselves to appropriate aspects of external environmental events and internal operations. Attention facilitates the selection of salient information and the allocation of cognitive processing appropriate to that information. Attention is not a unitary process that can be localized to a single neuroanatomical region. Before the cortical registration of sensory information, activation of important subcortical structures occurs, which is called as an orienting response. Once sensory information reaches the sensory cortex, a large number of perceptual processes occur, which provide various levels of perceptual resolution of the critical features of the stimuli. After this preattentional processing, information is integrated within higher cortical(heteromodal) systems in inferior parietal and temporal lobes. At this stage, the processing characteristics can be modified, and the biases of the system have a direct impact on attentional selection. Information flow has been traced through sensory analysis to a processing stage that enables the new information to be focused and modified in relation to preexisting biases. The limbic and paralimbic system play significant roles in modulating attentional response. It is labeled with affective salience and is integrated according to ongoing pressures from the motivational drive system of the hypothalamus. The salience of information greatly influences the allocation of attention. The frontal lobe operate response selection system with a reciprocal interaction with both the attention system of the parietal lobe and the limbic system. In this attentional process, the search with the spatial field is organized and a sequence of attentional responses is generated. Affective, motivational and appectitive impulses from limbic system and hypothalamus trigger response intention, preparation, planning, initiation and control of frontal lobe on this process. The reticular system, which produces ascending activation, catalyzes the overall system and increases attentional capacity. Also additional energetic pressures are created by the hypothalamus. As psychophysiological measurement, skin conductance, pupil diameter, muscle tension, heart rate, alpha wave of EEG can be used. Event related potentials also provide physiological evidence of attention during information process. NI component appears to be an electrophysiological index of selective attention. P3 response is developed during the attention related to stimulus discrimination, evaluation and response.

• The Korean Journal of Physiology
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• v.19 no.2
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• pp.227-232
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• 1985

Previously, we had reported that the electrical stimulation of peripheral nerve with stimlatory parameters of 20 V strength and 2 Hz frequency for 60 min resulted in reducing the pain reaction. The present study was performed to evaluate if the pain reaction was affected by the peripheral nerve stimulation with different stimulatory parameters in the decerebrated cat. The flexion reflex was used as an index of the pain reaction. The reflex was elicited by stimulating the sural nerve (stimulus strength of 20 $V\;\times\;0.5$msec) and recorded as a compound action potential from the motor nerve innervated to the posterior biceps femoris muscle. The common perneal nerve was selected as a peripheral nerve on which the electrical stimulation of various intensities and frequencies was applied. The results are summarized as follows : 1) The peripheral nerve stimulation with 100 mV strength, regardless of frequencies, did not affect the pain reaction induced by the sural nerve stimulation. 2) When the stimulus of 1V intensity and slow frequency (2 Hz) was applied to the peripheral nerve for 30 min or 60 min, the pain reaction was significantly reduced comparing to the control. However, this reduced pain reaction by the peripheral nerve stimulation was not reversed by the injection of naloxone (0.02 mg/kg) 3) High frequency stimulus (60 Hz) of 1V intensity for 30 or 60 min did not show any effects of affecting the pain reaction. These results suggest that the stimulus of relatively high intensity (at least 1V) and low frequency (2 Hz) is needed to elicite the analgesic effect by the peripheral nerve stimulation. By the 1V stimulus, $A\delta$ nerve fiber is activated. Therefore, an $A\delta$ or smaller nerve fibers must be activated for showing analgesia by the peripheral nerve stimulation. However, the mechanism of analgesia by the $A\delta$ nerve activation alone was not related to the endogeneous morphine system since the reduced pain reaction by the $A\delta$ fiber activation alone was not reversed by the treatment of naloxone.

• International Journal of Oral Biology
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• v.31 no.4
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• pp.113-118
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• 2006

In the primary sensory neuron of the mesencephalic trigeminal nucleus (MTN), the peripheral axon supplies a large number of annulospiral endings surrounding intrafusal fibers encapsulated in single muscle spindles while the central axon sends only a few number of synapses onto single ${\alpha}-motoneurons({\alpha}-MNs)$. Therefore, the ${\alpha}-{\gamma}$ linkage is thought to be very crucial in the jaw-closing movement. Spike activity in a ${\gamma}-motoneuron\;({\gamma}-MN)$ would induce a large number of impulses in single peripheral axons by activating many intrafusal fibers simultaneously, subsequently causing an activation of ${\alpha}-MNs$ in spite of the small number of synapses. Thus, the activity of ${\gamma}-MNs$ may be vital for modulation of jaw-closing movements. Independently of such a spindle activity modulated by ${\gamma}-MNs$, somatic depolarization in MTN neurons is known to trigger the oscillatory spike activity. Nevertheless, the trafficking of these spikes arising from the two distinct sources of MTN neurons is not well understood. In this short review, switching among multiple functional modes of MTN neurons is discussed. Subsequently, it will be discussed which mode can support the ${\alpha}-{\gamma}$ linkage. In our most recent study, simultaneous patch-clamp recordings from the soma and axon hillock revealed a spike-back-propagation from the spike-initiation site in the stem axon to the soma in response to a somatic current pulse. The persistent $Na^+$ current was found to be responsible for the spike-initiation in the stem axon, the activation threshold of which was lower than those of soma spikes. Somatic inputs or impulses arising from the sensory ending, whichever trigger spikes in the stem axon first, would be forwarded through the central axon to the target synapse. We also demonstrated that at hyperpolarized membrane potentials, 4-AP-sensitive $K^+$ current ($IK_{4-AP}$) exerts two opposing effects on spikes depending on their origins; the suppression of spike initiation by increasing the apparent electrotonic distance between the soma and the spike-initiation site, and the facilitation of axonal spike invasion at higher frequencies by decreasing the spike duration and the refractory period. Through this mechanism, the spindle activity caused by ${\gamma}-MNs$ would be safely forwarded to ${\alpha}-MNs$. Thus, soma spikes shaped differentially by this $IK_{4-AP}$ depending on their origins would reflect which one of the two inputs was forwarded to the target synapses.

• Archives of Pharmacal Research
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• v.24 no.6
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• pp.546-551
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• 2001

We have previously shown that, in circular muscle cells of the lower esophageal sphincter (LES) isolated by enzymatic digestion, contraction in response to maximally effective doses of acetylcholine (ACh) or Inositol Triphosphate ($IP_3$) depends on the release of $Ca^{2+}$ from intracellular stores and activation of a $Ca6{2+}$-calmodulin (CaM)-dependent pathway. On the contrary, maintenance of LES tone, and response to low doses of ACh or $IP_3$ depend on a protein kinase C (PKC) mediated pathway. In the present investigation, we have examined requirements for $Ca6{2+}$ regulation of the interaction between CaM- and PKC-dependent pathways in LES contraction. Thapsigargin (TG) treatment for 30 min dose dependently reduced ACh-induced contraction of permeable LES cells in free $Ca6{2+}$ medium. ACh-induced contraction following the low level of reduction of $Ca6{2+}$ stores by a low dose of TG ($10^{-9}{\;}M$) was blocked by the CaM antagonist, CCS9343B but not by the PKC antagonists chelerythrine or H7, indicating that the contraction is CaM-dependent. After maximal reduction in intracellular $Ca{2+}$ from $Ca6{2+}$stores by TG ($10^{-6}{\;}M$), ACh-induced contraction was blocked by chelerythrine or H7, but not by CCS9343B, indicating that it is PKC-dependent. In normal $Ca^{2+}$medium, the contraction by ACh after TG ($10^{-9}{\;}M$) treatment was also CaM-dependent, whereas the contraction by ACh after TG ($10^{-9}{\;}M$) treatment was PKC-dependent. We examined whether PKC activation was inhibited by activated CaM. CCS 7343B Inhibited the CaM-induced contraction, but did not inhibit the DAC-induced contraction. CaM inhibited the DAC-induced contraction in the presence of CCS 9343B. This inhibition by CaM was $Ca{2+}$dependent. These data are consistent with the view that the switch from a PKC-dependent pathway to a CaM dependent pathway can occur and can be regulated by cytosolic $Ca{2+}$ in the LES.

• The Korean Journal of Physiology and Pharmacology
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• v.27 no.2
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• pp.143-155
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• 2023

Percutaneous coronary intervention and acute coronary syndrome are both closely tied to the frequently occurring complication of coronary microembolization (CME). Resveratrol (RES) has been shown to have a substantial cardioprotective influence in a variety of cardiac diseases, though its function and potential mechanistic involvement in CME are still unclear. The forty Sprague-Dawley rats were divided into four groups randomly: CME, CME + RES (25 mg/kg), CME + RES (50 mg/kg), and sham (10 rats per group). The CME model was developed. Echocardiography, levels of myocardial injury markers in the serum, and histopathology of the myocardium were used to assess the function of the cardiac muscle. For the detection of the signaling of TLR4/MyD88/NF-κB along with the expression of pyroptosis-related molecules, ELISA, qRT-PCR, immunofluorescence, and Western blotting were used, among other techniques. The findings revealed that myocardial injury and pyroptosis occurred in the myocardium following CME, with a decreased function of cardiac, increased levels of serum myocardial injury markers, increased area of microinfarct, as well as a rise in the expression levels of pyroptosis-related molecules. In addition to this, pretreatment with resveratrol reduced the severity of myocardial injury after CME by improving cardiac dysfunction, decreasing serum myocardial injury markers, decreasing microinfarct area, and decreasing cardiomyocyte pyroptosis, primarily by blocking the signaling of TLR4/MyD88/NF-κB and also reducing the NLRP3 inflammasome activation. Resveratrol may be able to alleviate CME-induced myocardial pyroptosis and cardiac dysfunction by impeding the activation of NLRP3 inflammasome and the signaling pathway of TLR4/MyD88/NF-κB.