• 제목/요약/키워드: Activation Channels

검색결과 268건 처리시간 0.027초

External pH Effects on Delayed Rectifier $K^+$ Currents of Small Dorsal Root Ganglion Neuron of Rat

  • Kim, Young-Ho;Hahn, Jung-Hyun;Lim, In-Ja;Chung, Sung-Kwon;Bang, Hyo-Weon
    • The Korean Journal of Physiology and Pharmacology
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    • 제2권2호
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    • pp.165-172
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    • 1998
  • Under certain pathophysiological conditions, such as inflammation and ischemia, the concentration of H^+$ ion in the tissue surrounding neurons is changed. Variations in H^+$ concentration are known to alter the conduction and/of the gating properties of several types of ion channels. Several types of K^+$ channels are modulated by pH. In this study, the whole cell configuration of the patch clamp technique has been applied to the recording of the responses of change of external pH on the delayed rectifier K^+$ current of cultured DRG neurons of rat. Outward K^+$ currents were examined in DRG cells, and the Charybdotoxin and Mn^{2+}$ could eliminate Ca^{2+}-dependent$ K^+$ currents from outward K^+$ currents. This outward K^+$ current was activated around -60 mV by step depolarizing pulses from holding potential -70 mV. Outward K^+$ currents were decreased by low external pH. Activation and steady-state inactivation curve were shifted to the right by acidification, while there was small change by alkalization. These results suggest that H^+$ could be alter the sensory modality by changing and modifying voltage-dependent K^+$ currents, which participated in repolarization.

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클러스터 형태의 다중 인터페이스 다중 홉 인지 라디오 네트워크를 위한 제어 채널 접근 기법 (A Control Channel Access Scheme for Clustered Multi-interface Multi-hop Cognitive Radio Networks)

  • 이지운;전화숙;정동근
    • 한국정보과학회논문지:정보통신
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    • 제37권4호
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    • pp.301-306
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    • 2010
  • 이 논문은 클러스터 형태의 다중 인터페이스 다중 홉 인지 라디오 환경을 위한 효율적인 제어 채널 접근 방식을 제안한다. 인지 라디오 대역 안에서 전체 네트워크 영역에 걸친 공통 채널을 확보하는 것이 어렵기 때문에, 대부분의 멀티 인터페이스 멀티 홉 인지 라디오 네트워크는 라이센스 사용자의 채널 사용 현황과 같은 제어 정보의 교환을 위해인지 라디오 대역 밖에 제어 채널을 두고 하나의 인터페이스를 제어 채널에 고정시켜 할당한다. 그러나 이러한 방식은 네트워크 인터페이스의 낭비를 초래한다. 이 연구는 인지 라디오 노드들이 다수의 데이터 채널을 통해 이웃 노드들과 연결되는 클러스터 구조 하에서 멀티 채널 상황에서의 숨겨진 노드 문제없이 데이터 채널과 제어 채널을 수시로 번갈아 가며 접근하는 방식에 대하여 고찰한다. 시뮬레이션을 사용하여 제안한 방식의 성능을 측정한다. 시뮬레이션 결과를 통해 제안한 방식이 하나의 네트워크 인터페이스를 제어 채널에 고정적으로 할당하여 데이터 전송을 하지 않는 방법에 비해 더 높은 네트워크 처리량을 보임을 확인한다.

Participation of $K_{ATP}$ Channels in the Antinociceptive Effect of Pregabalin in Rat Formalin Test

  • Kweon, Tae-Dong;Kim, Ji-Young;Kwon, Il-Won;Choi, Jong-Bum;Lee, Youn-Woo
    • The Korean Journal of Pain
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    • 제24권3호
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    • pp.131-136
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    • 2011
  • Background: Pregabalin is an anticonvulsant and analgesic agent that interacts selectively with the voltage-sensitive-$Ca^{2+}$-channel alpha-2-delta subunit. The aim of this study was to evaluate whether the analgesic action of intrathecal (IT) pregabalin is associated with KATP channels in the rat formalin test. Methods: IT PE-10 catheters were implanted in male Sprague-Dawley rats (250.300 g) under inhalation anesthesia using enflurane. Nociceptive behavior was defined as the number of hind paw flinches during 60 min after formalin injection. Ten min before formalin injection, IT drug treatments were divided into 3 groups: normal saline (NS) $20\;{\mu}l$ (CON group); pregabalin 0.3, 1, 3 and $10\;{\mu}g$ in NS $10\;{\mu}l$ (PGB group); glibenclamide $100\;{\mu}g$ in DMSO $5\;{\mu}l$ with pregabalin 0.3, 1, 3 and $10\;{\mu}g$ in NS $5\;{\mu}l$ (GBC group). All the drugs were flushed with NS $10\;{\mu}l$. Immunohistochemistry for the $K_{ATP}$ channel was done with a different set of rats divided into naive, NS and PGB groups. Results: IT pregabalin dose-dependently decreased the flinching number only in phase 2 of formalin test. The log dose response curve of the GBC group shifted to the right with respect to that of the PGB group. Immunohistochemistry for the $K_{ATP}$ channel expression on the spinal cord dorsal horn showed no difference among the groups 1 hr after the formalin test. Conclusions: The antinociceptive effect of pregabalin in the rat formalin test was associated with the activation of the $K_{ATP}$ channel. However, pregabalin did not induce $K_{ATP}$ channel expression in the spinal cord dorsal horn.

Inhibitory Effects of Dihydrexidine on Catecholamine Release from the Rat Adrenal Medulla

  • Lee, Jae-Hwang;Lim, Hyo-Jeong;Lim, Dong-Yoon
    • Biomolecules & Therapeutics
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    • 제17권1호
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    • pp.32-42
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    • 2009
  • The purpose of the present study was to examine the effect of dihydrexidine, a full $D_1$ receptor agonist, on the secretion of catecholamines (CA) from the perfused model of the rat adrenal gland, and to establish its mechanism of action. Dihydrexidine (10-100 ${\mu}M$), perfused into an adrenal vein for 60 min, relatively produced dose- and time-dependent inhibition in the CA secretory responses evoked by ACh (5.32 mM), high $K^+$ (56 mM), DMPP (100 ${\mu}M$) and McN-A-343 (100 ${\mu}M$). Dihydrexidine itself did fail to affect basal CA output. Also, in adrenal glands loaded with dihydrexidine (30 ${\mu}M$), the CA secretory responses evoked by Bay-K-8644 (10 ${\mu}M$), an activator of L-type $Ca^{2+}$ channels, cyclopiazonic acid (10 ${\mu}M$), an inhibitor of cytoplasmic $Ca^{2+}$-ATPase, and veratridine, an activator of voltage-dependent $Na+$ channels (10 ${\mu}M$), were also markedly inhibited, respectively. However, in the simultaneous presence of dihydrexidine (30 ${\mu}M$) and R (+)-SCH23390 (a selective antagonist of $D_1$ receptor, 3 ${\mu}M$), the CA secretory responses evoked by ACh, high K+, DMPP, McN-A-343, Bay-K-8644, cyclopiazonic acid and veratridine were considerably recovered to the extent of the corresponding control secretion compared with the inhibitory responses by dihydrexidinetreatment alone. In conclusion, these experimental results suggest that dihydrexidine significantly inhibits the CA secretion evoked by cholinergic stimulation (both nicotinic and muscarinic receptors) and membrane depolarization from the rat adrenal medulla. It seems that this inhibitory effect of dihydrexidine may be mediated by inhibiting influx of both $Ca^{2+}$ and $Na^+$ into the cytoplasm as well as by suppression of $Ca^{2+}$ release from cytoplasmic calcium store through activation of dopaminergic $D_1$ receptors located on the rat adrenomedullary chromaffin cells.

Decreased Voltage Dependent $K^+$ Currents in Cerebral Arterial Smooth Muscle Cells of One-Kidney, One-Clip Goldblatt Hypertensive Rat

  • Oh, Young-Sun;Kim, Se-Hoon;Kim, Hoe-Suk;Jeon, Byeong-Hwa;Chang, Seok-Jong;Kim, Kwang-Jin
    • The Korean Journal of Physiology and Pharmacology
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    • 제3권5호
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    • pp.471-479
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    • 1999
  • The Kv channel activity in vascular smooth muscle cell plays an important role in the regulation of membrane potential and blood vessel tone. It was postulated that increased blood vessel tone in hypertension was associated with alteration of Kv channel and membrane potential. Therefore, using whole cell mode of patch-clamp technique, the membrane potential and the 4-AP-sensitive Kv current in cerebral arterial smooth muscle cells were compared between normotensive rat and one-kidney, one-clip Goldblatt hypertensive rat (lK,lC-GBH rat). Cell capacitance of hypertensive rat was similar to that of normotensive rat. Cell capacitance of normotensive rat and 1K,lC-GBH rat were $20.8{\pm}2.3$ and $19.5{\pm}1.4$ pF, respectively. The resting membrane potentials measured in current clamp mode from normotensive rat and 1K,lC-GBH rat were $-45.9{\pm}1.7$ and $-38.5{\pm}1.6$ mV, respectively. 4-AP (5 mM) caused the resting membrane potential hypopolarize but charybdotoxin $(0.1\;{\mu}M)$ did not cause any change of membrane potential. Component of 4-AP-sensitive Kv current was smaller in 1K,lC-GBH rat than in normotensive rat. The voltage dependence of steady-state activation and inactivation of Kv channel determined by using double-pulse protocol showed no significant difference. These results suggest that 4-AP-sensitive Kv channels playa major role in the regulation of membrane potential in cerebral arterial smooth muscle cells and alterations of 4-AP-sensitive Kv channels would contribute to hypopolarization of membrane potential in 1K,lC-GBH rat.

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보건교육 정보시스템 개발에 관한 연구 (A Study on Structural Modeling of Activation of the Information System Utilization in the Health Education)

  • 김은주;김명;고승덕
    • 보건교육건강증진학회지
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    • 제15권1호
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    • pp.49-66
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    • 1998
  • The general objectives of this study were to develop a health education management information system to effectively deal with community health problems. This study aimed at 1) to development an health education management information system, and 2) to offer computer-based communication channels among the District Health System components such as health center, health subcenters, and community hospital, 3) lastly, to identify the key issues and effectiveness of health education. Major findings of the study were as follows: The major benefits and significances of this information system included: improvement of quality of health education statistics by reducing manual data processing, improvement of productivity of health educators by reducing paper works, improvement of decision-making capability of managers by providing more information for planning, organizing, and evaluating health education programes, and improvement of communication flow among health institutions. Based on the findings of the study, the following are recommended: (1) The health education information system will connect with computerized information systems of various health-related institutions in a district and computer-based communication channels among them, and of the superior agencies in the future. (2) The major functions of the computerized health education program are: to keep client medical records, to inquire about information on the client and his family's history. (3) The program will provide outputs in various forms, such as files for patient records, data on some chronic diseases, information on the patient and his family members, and various kinds of statistics.

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Calcium Signaling in Salivary Secretion

  • Kim, Jin Man;Lee, Sang-Woo;Park, Kyungpyo
    • Journal of Korean Dental Science
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    • 제10권2호
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    • pp.45-52
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    • 2017
  • Calcium has versatile roles in diverse physiological functions. Among these functions, intracellular $Ca^{2+}$ plays a key role during the secretion of salivary glands. In this review, we introduce the diverse cellular components involved in the saliva secretion and related dynamic intracellular $Ca^{2+}$ signals. Calcium acts as a critical second messenger for channel activation, protein translocation, and volume regulation, which are essential events for achieving the salivary secretion. In the secretory process, $Ca^{2+}$ activates $K^+$ and $Cl^-$ channels to transport water and electrolyte constituting whole saliva. We also focus on the $Ca^{2+}$ signals from intracellular stores with discussion about detailed molecular mechanism underlying the generation of characteristic $Ca^{2+}$ patterns. In particular, inositol triphosphate signal is a main trigger for inducing $Ca^{2+}$ signals required for the salivary gland functions. The biphasic response of inositol triphosphate receptor and $Ca^{2+}$ pumps generate a self-limiting pattern of $Ca^{2+}$ efflux, resulting in $Ca^{2+}$ oscillations. The regenerative $Ca^{2+}$ oscillations have been detected in salivary gland cells, but the exact mechanism and function of the signals need to be elucidated. In future, we expect that further investigations will be performed toward better understanding of the spatiotemporal role of $Ca^{2+}$ signals in regulating salivary secretion.

Modeling of Arrhythmogenic Automaticity Induced by Stretch in Rat Atrial Myocytes

  • Youm, Jae-Boum;Leem, Chae-Hun;Zhang, Yin Hua;Kim, Na-Ri;Han, Jin;Earm, Yung-E.
    • The Korean Journal of Physiology and Pharmacology
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    • 제12권5호
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    • pp.267-274
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    • 2008
  • Since first discovered in chick skeletal muscles, stretch-activated channels (SACs) have been proposed as a probable mechano-transducer of the mechanical stimulus at the cellular level. Channel properties have been studied in both the single-channel and the whole-cell level. There is growing evidence to indicate that major stretch-induced changes in electrical activity are mediated by activation of these channels. We aimed to investigate the mechanism of stretch-induced automaticity by exploiting a recent mathematical model of rat atrial myocytes which had been established to reproduce cellular activities such as the action potential, $Ca^{2+}$ transients, and contractile force. The incorporation of SACs into the mathematical model, based on experimental results, successfully reproduced the repetitive firing of spontaneous action potentials by stretch. The induced automaticity was composed of two phases. The early phase was driven by increased background conductance of voltage-gated $Na^+$ channel, whereas the later phase was driven by the reverse-mode operation of $Na^+/Ca^{2+}$ exchange current secondary to the accumulation of $Na^+$ and $Ca^{2+}$ through SACs. These results of simulation successfully demonstrate how the SACs can induce automaticity in a single atrial myocyte which may act as a focus to initiate and maintain atrial fibrillation in concert with other arrhythmogenic changes in the heart.

Nootkatol prevents ultraviolet radiation-induced photoaging via ORAI1 and TRPV1 inhibition in melanocytes and keratinocytes

  • Woo, Joo Han;Nam, Da Yeong;Kim, Hyun Jong;Hong, Phan Thi Lam;Kim, Woo Kyung;Nam, Joo Hyun
    • The Korean Journal of Physiology and Pharmacology
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    • 제25권1호
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    • pp.87-94
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    • 2021
  • Skin photoaging occurs due to chronic exposure to solar ultraviolet radiation (UV), the main factor contributing to extrinsic skin aging. Clinical signs of photoaging include the formation of deep, coarse skin wrinkles and hyperpigmentation. Although melanogenesis and skin wrinkling occur in different skin cells and have different underlying mechanisms, their initiation involves intracellular calcium signaling via calcium ion channels. The ORAI1 channel initiates melanogenesis in melanocytes, and the TRPV1 channel initiates MMP-1 production in keratinocytes in response to UV stimulation. We aimed to develop a drug that may simultaneously inhibit ORAI1 and TRPV1 activity to help prevent photoaging. We synthesized nootkatol, a chemical derivative of valencene. TRPV1 and ORAI1 activities were measured using the whole-cell patch-clamp technique. Intracellular calcium concentration [Ca2+]i was measured using calcium-sensitive fluorescent dye (Fura-2 AM). UV-induced melanin formation and MMP-1 production were quantified in B16F10 melanoma cells and HaCaT cells, respectively. Our results indicate that nootkatol (90 μM) reduced TRPV1 current by 94% ± 2% at -60 mV and ORAI1 current by 97% ± 1% at -120 mV. Intracellular calcium signaling was significantly inhibited by nootkatol in response to ORAI1 activation in human primary melanocytes (51.6% ± 0.98% at 100 μM). Additionally, UV-induced melanin synthesis was reduced by 76.38% ± 5.90% in B16F10 melanoma cells, and UV-induced MMP-1 production was reduced by 59.33% ± 1.49% in HaCaT cells. In conclusion, nootkatol inhibits both TRPV1 and ORAI1 to prevent photoaging, and targeting ion channels may be a promising strategy for preventing photoaging.

Regulatory mechanisms of the store-operated Ca2+ entry through Orai1 and STIM1 by an adaptor protein in non-excitable cells

  • Kang, Jung Yun;Yang, Yu-Mi
    • International Journal of Oral Biology
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    • 제47권3호
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    • pp.33-40
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    • 2022
  • Store-operated Ca2+ entry (SOCE) represents one of the major Ca2+ entry routes in non-excitable cells. It is involved in a variety of fundamental biological processes and the maintenance of Ca2+ homeostasis. The Ca2+ release-activated Ca2+ (CRAC) channel consists of stromal interaction molecule and Orai; however, the role and action of Homer proteins as an adaptor protein to SOCE-mediated Ca2+ signaling through the activation of CRAC channels in non-excitable cells still remain unknown. In the present study, we investigated the role of Homer2 in the process of Ca2+ signaling induced by the interaction between CRACs and Homer2 proteins in non-excitable cells. The response to Ca2+ entry by thapsigargin-mediated Ca2+ store depletion remarkably decreased in pancreatic acinar cells of Homer2-/- mice, as compared to wild-type cells. It also showed critical differences in regulated patterns by the specific blockers of SOCE in pancreatic acinar cells of Homer2-/- mice. The response to Ca2+ entry by the depletion in Ca2+ store markedly increased in the cellular overexpression of Orai1 and STIM1 as compared to the overexpression of Homer2 in cells; however, this response was remarkably inhibited by the overexpression of Orai1, STIM1, and Homer2. These results suggest that Homer2 has a critical role in the regulatory action of SOCE activity and the interactions between CRAC channels.