• 한국생물물리학회:학술대회논문집
• /
• 한국생물물리학회 1999년도 학술발표회 진행표 및 논문초록
• /
• pp.61-62
• /
• 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.

• 한국콘텐츠학회논문지
• /
• 제9권9호
• /
• pp.278-286
• /
• 2009

본 연구는 스트레칭이 $\alpha$-운동신경원의 흥분도를 변화시키는지의 여부와 이에 따른 유연성의 변화 정도를 알아보고자 시도되었다. 본 연구에서 $\alpha$-운동신경원 흥분도는 비복근 H-반사의 Hmax/Mmax 비로 측정하였으며 근육의 유연성은 족관절의 능동 배측굴곡 가동 범위를 통해 알아보았다. 스트레칭은 10명의 건강한 피검자를 대상으로 총 4분간(2분간의 스트레칭, 1분의 휴식, 2분간의 스트레칭), 각 시기별로 비복근에 적용하였다. $\alpha$-운동신경원 흥분도와 유연성을 분석하기 위해 본 연구에서는 스트레칭 적용 전, 1차 스트레칭 적용 직후, 2차 스트레칭 적용 직후, 그리고 2차 스트레칭 적용 후 48시간 후 Hmax/Hmax와 족관절의 능동 배측굴곡 각도를 측정하였다. 본 연구의 결과 1차와 2차 스트레칭 적용 후 의미 있는 $\alpha$-운동신경원 흥분도의 감소와 족관절 능동 배측굴곡 각도의 증가가 나타났으나 스트레칭을 소거한 48시간 후에는 $\alpha$-운동신경원 흥분도와 족관절의 능동 배측굴곡 가동 범위가 스트레칭 적용전과 비슷한 상태로 되돌아갔다. 이러한 스트레칭에 의한 비복근 $\alpha$-운동신경원 흥분도 감소와 이에 따른 족관절 배측굴곡 유연성 증가는 족관절 주변의 III형 기계적 수용기와 근육에 위치한 골지건 기관의 활성 결과로 사료된다.

• 한국산학기술학회논문지
• /
• 제22권2호
• /
• pp.659-666
• /
• 2021

이 연구는 정상 성인에서 머리-목 굽힘 운동 시 시선의 각도와 압력이 깊은목굽힘근의 두께변화에 미치는 영향을 알아보고자 하였다. 본 연구에는 27명이 참여하였다. 머리-목굽힘 운동하는 동안 4가지(0°, 20°, 40°, 60°)의 시선과 5가지(20mmHg, 22mmHg, 24mmHg, 26mmHg, 28mmHg)의 압력에서 목긴근과 목빗근의 근 두께는 초음파 영상을 이용해 측정하였다. 시선 각도 및 압력변화에 따른 목긴근과 목빗근의 두께 변화를 비교 분석하기 위하여 반복측정분산분석을 수행하였다. 본 연구결과, 목긴근은 20과 22mmHg에서 0°와 20°, 0°와 40°, 0°와 60°은 유의한 차이를 보였으며, 20°에서 가장 근활성도가 높았다(p<.05). 목빗근은 28mmHg에서 0°와 20°, 20°와 40°, 40°와 60°은 유의한 차이를 보였으며, 20°에서 가장 낮은 근활성도를 보였다(p<.05). 본 연구에서 머리-목 굽힘 운동 시에는 시선의 방향을 20°로 설정하는 것이 목긴근의 활성화를 높이고, 목빗근의 근활성도를 낮추어 운동의 효과를 얻을 수 있다는 것을 찾았다. 본 연구의 결과를 바탕으로 임상환경에서 머리-목 굽힘 운동시에 시선 방향을 설정하여 운동의 효과를 증대시키길 바란다.

• The Korean Journal of Physiology and Pharmacology
• /
• 제26권4호
• /
• pp.277-285
• /
• 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
• /
• 제40권4호
• /
• pp.261-266
• /
• 2010

미토콘드리아에서 생성하는 ATP는 미토콘드리아의 속막에 존재하는 전자전달계 효소(electron transferase)에 의해 생성되며, 이러한 전자전달계 효소는 복합체 I, II, III, IV, V로 구성되어 있다고 알려져 있다. ATP는 ATPase에 의해 생성되며, ATPase는 $F_0$와 $F_1$ 소복합체로 구성되어 있다. 미토콘드리아의 외막에는 Porin 또는 VDAC(voltage-dependent anion-selective channel)이라고 알려져 있는 미세한 구멍 형태의 단백질이 존재하며, 세포질에 존재하는 succinate, malate, ATP와 같은 음전하용질 또는 전자를 선택적으로 통과시키는 역할을 수행하는 것으로 보고된 바 있다. 본 연구에서는 소의 심근 미토콘드리아에 존재하고 있는 porin과 ATPase의 기능과 분포의 관계를 알아보기 위하여, porin과 ATPase Ⅴ-${\beta}$ 항체를 면역반응법을 이용한 광학현미경과 이중면역반응법을 이용한 형광현미경으로 확인하고, 심근 미토콘드리아의 두 단백질 분포를 면역황금표지법을 이용한 전자현미경으로 관찰하였다. 미토콘드리아에서 porin 항체에 대한 미토콘드리아 조직항원의 발색은 조직내에서 전반적으로 관찰할 수 있었으며, ATPase 항체에 대한 조직항원의 발색은 세로면에서 관찰되었다. 이중면역응법에서 porin 항체와 ATPase는 각각 다른 조직에서 발색이 관찰되거나, 같은 조직 내에서 관찰되었다. 면역황금표지법에서 porin 항체는 미토콘드리아의 바깥막에서 황금입자가 표지된 것을 확인할 수 있었으며, ATPase는 미토콘드리아의 속막에서 황금입자가 표지된 것을 확인할 수 있었다. 그러나 ATPase 항체가 황금입자로 표지되지 않은 미토콘드리아도 확인되었다. 이러한 결과로 porin 항체와 ATPase 항체는 미토콘드리아의 바깥막과 속막에 각각 분포양상을 확인하였다. porin 항체의 발색으로 인한 조직 내의 미토콘드리아가 존재하고 있음을 확인할 수 있었으며, ATPase 항체의 발색으로 인한 ATP를 생성하는 미토콘드리아를 확인할 수 있었다. 하지만 porin 항체의 반응으로 확인된 미토콘드리아가 반드시 ATP를 생성하는 것은 아니라는 것을 추측할 수 있었다.

• 수면정신생리
• /
• 제5권2호
• /
• pp.119-133
• /
• 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
• /
• 제19권2호
• /
• pp.227-232
• /
• 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
• /
• 제31권4호
• /
• pp.113-118
• /
• 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
• /
• 제24권6호
• /
• pp.546-551
• /
• 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
• /
• 제27권2호
• /
• pp.143-155
• /
• 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.