감각신경계의 신경생리와 임상적 이용

서대원 대한임상신경생리학회 2010 Annals of Clinical Neurophysiology Vol.12 No.2

Various electrophysiological tests have provided a large body of valuable information on neuronal responses to a presented stimulus. The special and general somatic sensory pathways are main targets of evoked potentials. Two types of evoked potentials, exogenous and endogenous, are commonly used. Exogenous evoked potentials of general and special somatic sensory systems will be reviewed. One of general somatic sensory functional pathways, proprioception, can be evaluated by general somatosensory evoked potentials with electrical stimulation on nerves. The special somatosensory functional pathways,including vision, and audition, can be evaluated by visual evoked potentials and auditory evoked potentials. Also laser-evoked potentials are newly developed for pain pathway, including lateral spinothalamic pathway, and vestibular myogenic evoked potentials for sacculocollic pathways. The evoked potentials of sensory system have maximal clinical utility in evaluating functional deficits along the sensory pathways. They are used for evaluating comatose patients, hysterical patients, premature infants, patients with suspected demyelinating diseases or neoplasms, and research. We discuss the neurophysiologic tests of sensory systems in views of practical points. The organized evaluation of sensory electrophysiologic tests can be helpful in detecting and estimating the abnormalities in neurological diseases.

Exactly Solvable Potentials Derived from SWKB Quantization

Sun, Hosung Korean Chemical Society 2014 Bulletin of the Korean Chemical Society Vol.35 No.3

The shape invariant potentials are proved to be exactly solvable, i.e. the wave functions and energies of a particle moving under the influence of the shape invariant potentials can be algebraically determined without any approximations. It is well known that the SWKB quantization is exact for all shape invariant potentials though the SWKB quantization itself is approximate. This mystery has not been mathematically resolved yet and may not be solved in a concrete fashion even in the future. Therefore, in the present work, to understand (not prove) the mystery an attempt of deriving exactly solvable potentials directly from the SWKB quantization has been made. And it turns out that all the derived potentials are shape invariant. It implicitly explains why the SWKB quantization is exact for all known shape invariant potentials. Though any new potential has not been found in this study, this brute-force derivation of potentials helps one understand the characteristics of shape invariant potentials.

Exactly Solvable Potentials Derived from SWKB Quantization

선호성 대한화학회 2014 Bulletin of the Korean Chemical Society Vol.35 No.3

The shape invariant potentials are proved to be exactly solvable, i.e. the wave functions and energies of a particle moving under the influence of the shape invariant potentials can be algebraically determined without any approximations. It is well known that the SWKB quantization is exact for all shape invariant potentials though the SWKB quantization itself is approximate. This mystery has not been mathematically resolved yet and may not be solved in a concrete fashion even in the future. Therefore, in the present work, to understand (not prove) the mystery an attempt of deriving exactly solvable potentials directly from the SWKB quantization has been made. And it turns out that all the derived potentials are shape invariant. It implicitly explains why the SWKB quantization is exact for all known shape invariant potentials. Though any new potential has not been found in this study, this brute-force derivation of potentials helps one understand the characteristics of shape invariant potentials.

Hwangryunhaedok-tang induces the depolarization of pacemaker potentials through 5-HT ₃ and 5-HT ₄ receptors in cultured murine small intestine interstitial cells of Cajal

Kim, Hyun Jung,Lee, Guem San,Kim, Hyungwoo,Kim, Byung Joo WJG Press 2017 WORLD JOURNAL OF GASTROENTEROLOGY Vol.23 No.29

<P><B>AIM</B></P><P>To investigate the effects of a water extract of Hwangryunhaedok-tang (HHTE) on the pacemaker potentials of mouse interstitial cells of Cajal (ICCs).</P><P><B>METHODS</B></P><P>We dissociated ICCs from small intestines and cultured. ICCs were immunologically identified using an anti-c-kit antibody. We used the whole-cell patch-clamp configuration to record the pacemaker potentials generated by cultured ICCs under the current clamp mode (<I>I</I> = 0). All experiments were performed at 30 °C-32 °C</P><P><B>RESULTS</B></P><P>HHTE dose-dependently depolarized ICC pacemaker potentials. Pretreatment with a 5-HT<SUB>3</SUB> receptor antagonist (Y25130) or a 5-HT<SUB>4</SUB> receptor antagonist (RS39604) blocked HHTE-induced pacemaker potential depolarizations, whereas pretreatment with a 5-HT<SUB>7</SUB> receptor antagonist (SB269970) did not. Intracellular GDPβS inhibited HHTE-induced pacemaker potential depolarization and pretreatment with a Ca<SUP>2+</SUP>-free solution or thapsigargin abolished the pacemaker potentials. In the presence of a Ca<SUP>2+</SUP>-free solution or thapsigargin, HHTE did not depolarize ICC pacemaker potentials. In addition, HHTE-induced pacemaker potential depolarization was unaffected by a PKC inhibitor (calphostin C) or a Rho kinase inhibitor (Y27632). Of the four ingredients of HHT, Coptidis Rhizoma and Gardeniae Fructus more effectively inhibited pacemaker potential depolarization.</P><P><B>CONCLUSION</B></P><P>These results suggest that HHTE dose-dependently depolarizes ICC pacemaker potentials through 5-HT<SUB>3</SUB> and 5-HT<SUB>4</SUB> receptors <I>via</I> external and internal Ca<SUP>2+</SUP> regulation and <I>via</I> G protein-, PKC- and Rho kinase-independent pathways.</P>

1, 4-Dihydropyridine 칼슘길항제가 유두근의 정상활동전압 및 Ca-dependent, Slow Channel Mediated Action Potential에 미치는 영향

김민형,장석종,Kim, Min-Hyung,Chang, Seok-Jong 대한생리학회 1988 대한생리학회지 Vol.22 No.2

Effects of 1, 4-dihydropyridine compounds, such as nifedipine, nisoldipine, nitrendipine, and nimodipine which were calcium antagonists on the normal and Ca-dependent, slow channel mediated action potentials in the guinea pig's papillary muscle were investigated. The glass microelectrode was impaled into a papillary muscle cell for measurements of potential changes with the simultaneous tracing of isometric contraction. The concentration of Ca antagonists were 1 mg/l (nifedipine and nisoldipine), 2 mg/l (nitrendipine and nimodipine), which showed the maximal inhibition of isometric contraction (above 90%) and simultaneous effects on the normal action potentials and only the halves of those concentrations were sufficient to observe the effects on the calcium action potentials. The data for analysis were only chosen when the microelectrode was maintained in a cell throughout the experiments. 1, 4-Dihydropyridine compounds decreased the action potential duration but did not affect the resting membrane potential, overshoot, and upstroke velocity of the normal action potentials with the decrease in the isometric contraction. And with the decrease in the area and amplitude of isometric contraction, the area, amplitude, upstroke velocity and duration of Ca action potential was decreased. But the differences in the effects of the Ca antagonists were not observed. Therefore it is inferred that the changes in normal and Ca action potential induced by the 1, 4-dihydropyridine compounds with a common chemical structure would be caused by the slow inward Ca-current, not by a fast Na-current.

Sphenoidal ERPs의 임상적 유용성에 관한 연구

송대원,서만욱,김영현 의과학연구소 1997 全北醫大論文集 Vol.21 No.1

The P300 component of the event-related potential(ERP) has been studied extensively since its discovery by Sutton and his colleagues. The P3 event-related potential(ERP) may be elicited in a task where subjects are required to discriminate between two types of stimuli, one of which is presented infrequently. Although the best combination of electrophysiologic studies has not yet been defined(National institute of health, 1990), this method appears to be important because it is safe and reproducible and provides easy access to all patients evaluated for epilepsy surgery. These data provide guidance in the clinical use of limbic P3s in the presurgical localization of epileptogenic foci. The finding of a unilateral absent P3 ipsilateral to the presumed temporal seizure focus provides strong supproting evidence for the epileptogenicity of that temporal love with a sensitivity and specificity of 81% and 95%, respectively. In summary, our data showed that the common finding in intractable TLE(Temporal lobe epilepsy) was a unilaterally absent limbic P3. This finding correlated strongly with the side of the seizure focus and hippocampal sclerosis was the usual pathologic substrate. Determination of the limbic P3 can add weight to the decition to operate if it is unilaterally absent on the putative epileptogenic side. Endogenous electrical potentials appear at the sclap when a subject is engaged in taske requiring judgements about the properties of a stimulus. Typically, the component of task-related potentials appear between about 200 and 600 msec after the onset of the stimulus. The strengths of these components depend mainly on the relevance of the stimulus to the task and less on the sensory modality being stimulated or on the particular sensory properties of the stimulus. Owing to the risks entailed in intracerebral depth electrode implantation, less invasive procedures are desirable. Meador et al reported a significant relationship between limbic evoked potentiala(LEPs) recorded from intreacerebral depth electrodes and the site of seizure onset. We investigated application of a similar EP technique using sphenoidal electrodes. Sphenoidal electrodes are safe and are superior to scalp electrodes in recording EEG from the inferior mesial temporal lobes. The present study is a prospective investigation of the relationship of the side of temporal lobe seizure onset to the spectral power of the sphenoidal-temporal target evoked potentials. Based on our studies of hippocampal LEPs, we postulated that spectral power of the sphenoidal evoked potentials woud be reduced on the side of seizure onset. key Words : Epilepsy, Spenoidal elecrodes, Event-related potentials

생쥐 소장 카할세포의 pacemaker potential에서 미르타자핀 효능에 관한 연구

김병주(Byung Joo Kim) 한국생명과학회 2021 생명과학회지 Vol.31 No.7

카할세포는 위장관 근육의 pacemaker 세포이다. 이번 연구는 생쥐 소장에서 얻은 카할세포를 배양하여 노르아드레날린성 및 세로토닌성 항우울제인 미르타자핀의 효과를 조사했다. 전기생리학적인 방법을 이용하여 카할세포의 pacemaker potential의 변화를 측정하였다. 미르타자핀은 농도 의존적 방식으로 카할세포 탈분극을 일으켰다. Y25130 (5-HT3 수용체 길항제), RS39604 (5-HT4 수용체 길항제) 또는 SB269970 (5-HT7 수용체 길항제)은 미르타자핀에 의한 카할세포 탈분극에 영향을 미치지 않았다. 또한, 무스카린성 M2 수용체 길항제인 메톡 트라민은 미르타자핀에 의한 카할세포의 탈분극에 영향을 미치지 않은 반면, 무스카린성 M3 수용체 길항제인 4-DAMP는 카할세포의 탈분극을 억제하였다. GDP-β-S를 피펫을 통해 카할세포내로 넣었을 때, 미르타자핀에 카할세포 탈분극이 억제되었다. 외부에 칼슘이 없는 용액 또는 소포체의 Ca<SUP>2+</SUP>-ATPase 억제제인 thapsigargin이 있는 경우 미르타자핀에 의한 카할세포 탈분극이 나타났다. 또한, protein kinase C (PKC) 억제제인 칼포스틴 C 또는 chelerythrine은 미르타자핀에 의한 탈분극을 억제했습니다. 이러한 결과는 미르 타자핀이 카할세포에서 G 단백질 및 PKC 경로에 의한 무스카린성 M3 수용체 활성화를 통해 탈분극을 조절 함을 알 수 있다. 따라서 미르타자핀이 카할세포를 통해 위장관 운동성을 조절할 수 있음을 시사한다. Interstitial cells of Cajal (ICCs) are the pacemaking cells in the gastrointestinal (GI) muscles that generate the rhythmic oscillation in membrane potentials known as slow waves. In the present study, we investigated the effects of mirtazapine, a noradrenergic and serotonergic antidepressant, on pacemaking potential in cultured ICCs from the murine small intestine. The whole-cell patch-clamp configuration was used to record pacemaker potential in cultured ICCs. Mirtazapine induced pacemaker potential depolarizations in a concentration-dependent manner in the current clamp mode. Y25130 (a 5-HT3 receptor antagonist), RS39604 (a 5-HT4 receptor antagonist), and SB269970 (a 5-HT7 receptor antagonist) had no effects on mirtazapine-induced pacemaker potential depolarizations. Also, methoctramine, a muscarinic M₂ receptor antagonist, had no effect on mirtazapine-induced pacemaker potential depolarizations, whereas 4-diphenylacetoxy-N-methyl-piperidine methiodide (4-DAMP), a muscarinic M₃ receptor antagonist, inhibited the depolarizations. When guanosine 5"-[β-thio] diphosphate (GDP-β-S; 1 mM) was in the pipette solution, mirtazapine-induced pacemaker potential depolarization was blocked. When an external Ca<SUP>2+</SUP> free solution or thapsigargin, a Ca<SUP>2+</SUP>-ATPase inhibitor of the endoplasmic reticulum, was applied, the generation of pacemaker potentials disappeared, and under these conditions, mirtazapine induced pacemaker potential depolarizations. In addition, protein kinase C (PKC) inhibitor, calphostin C, and chelerythrine inhibited mirtazapine-induced pacemaker potential depolarizations. These results suggest that mirtazapine regulates pacemaker potentials through muscarinic M₃ receptor activation via a G protein-dependent and an external or internal Ca<SUP>2+</SUP>-independent PKC pathway in the ICCs. Therefore, mirtazapine can control GI motility through ICCs.

홍화의 생쥐 소장 및 대장 카할 간질세포의 향도잡이 전위 조절에 미치는 효능에 관한 연구

김병주 대한한의학방제학회 2019 大韓韓醫學方劑學會誌 Vol.27 No.4

Objectives : The purpose of this study was to investigate the effects of Carthami flos on pacemaker potentials of small intestinal and colonic Interstitial Cells of Cajal (ICC). Methods : To dissociate the ICC, we used enzymatic digestions from the small intestine and colon in mice. In the ICC, the electrophysiological whole-cell patch-clamp configuration was used to record pacemaker potentials in the cultured ICC. Results : 1. The ICC generated pacemaker potentials in the murine small intestine and colon. 2. Pretreatment with a Ca2+ free solution and thapsigargin, a Ca2+-ATPase inhibitor in the endoplasmic reticulum, stopped the pacemaker potentials. In the case of Ca2+-free solutions, Carthami flos did not induce membrane depolarizations in the murine small intestine and colon. However, when thapsigargin in a bath solution was applied, Carthami flos induced membrane depolarizations only in the murine colon. 3. Pretreatment with 2-APB (transient receptor potential melastatin (TRPM) channel inhibitor) abolished the pacemaker potentials and suppressed Carthami flos-induced effects in the murine small intestine and colon. 4. However, pretreatment with T16Ainh-AO1 (Ca2+ activated Cl- channel; anoctamin 1 (ANO1) inhibitor) did not affect the pacemaker potentials and induced Carthami flos-induced effects only in the murine small intestine. Conclusions : These results suggest that Carthami flos can modulate the pacemaker activity of ICC and the mechanisms underlying pacemaking in ICC might be different in the small intestine and the colon.

이진탕의 생쥐 소장 카할세포 향도잡이 전압에 미치는 효능에 관한 연구

한동훈,김정남,김병주 대한한의학방제학회 2020 大韓韓醫學方劑學會誌 Vol.28 No.1

Obejectives : The purpose of this study was to investigate the effects of Yijin-tang on pacemaker potentials of small intestinal interstitial Cells of Cajal (ICC). Methods : To dissociate the ICC, we used enzymatic digestions from the small intestine in mice. The electrophysiological whole-cell patch-clamp configuration was used to record pacemaker potentials in the cultured ICC and the in vivo effects of Yijin-tang on GI motility were investigated by calculating percent intestinal transit rates (ITR). Results : 1. The ICC generated pacemaker potentials in the murine small intestine. Yijin-tang produced membrane depolarization with concentration-dependent manners in the current clamp mode. 2. Pretreatment with a Ca2+ free solution and thapsigargin, a Ca2+-ATPase inhibitor in the endoplasmic reticulum, stopped the pacemaker potentials. In the case of Ca2+-free solutions and thapsigargin, Yijin-tang did not induce membrane potential depolarizations. 3. U73122, a phospholipase C (PLC) inhibitors, blocked the Yijin-tang-induced membrane potential depolarizations. However, U73343, an inactive PLC inhibitors, did not block. 4. In the presence of protein kinase C (PKC) inhibitors, staurosporine or Rottlerin, Yijin-tang depolarized the pacemaker potentials. However, in the presence of Go6976, Yijin-tang did not depolarize the pacemaker potentials. 5. In mice, intestinal transit rate (ITR) values were significantly and dose-dependently increased by the intragastric administration of Yijin-tang. Conclusions : These results suggest that Yijin-tang can modulate the pacemaker activity of ICC through an internal/external Ca2+ and PLC/PKC-dependent pathway in ICC. In addition, Yijin-tang is a good candidate for the development of a prokinetic agent.

The Mechanism of Action of Ghrelin and Motilin in the Pacemaker Potentials of Interstitial Cells of Cajal from the Murine Small Intestine

김정남,김병주 한국분자세포생물학회 2019 Molecules and cells Vol.42 No.6

Interstitial cells of Cajal (ICCs) are pacemaker cells that exhibit periodic spontaneous depolarization in the gastrointestinal (GI) tract and generate pacemaker potentials. In this study, we investigated the effects of ghrelin and motilin on the pacemaker potentials of ICCs isolated from the mouse small intestine. Using the whole-cell patch-clamp configuration, we demonstrated that ghrelin depolarized pacemaker potentials of cultured ICCs in a dose-dependent manner. The ghrelin receptor antagonist [D-Lys] GHRP-6 completely inhibited this ghrelin-induced depolarization. Intracellular guanosine 5'-diphosphate-β-S and pre-treatment with Ca2+-free solution or thapsigargin also blocked the ghrelin-induced depolarization. To investigate the involvement of inositol triphosphate (IP3), Rho kinase, and protein kinase C (PKC) in ghrelin-mediated pacemaker potential depolarization of ICCs, we used the IP3 receptor inhibitors 2-aminoethoxydiphenyl borate and xestospongin C, the Rho kinase inhibitor Y-27632, and the PKC inhibitors staurosporine, Go6976, and rottlerin. All inhibitors except rottlerin blocked the ghrelin-induced pacemaker potential depolarization of ICCs. In addition, motilin depolarized the pacemaker potentials of ICCs in a similar dose-dependent manner as ghrelin, and this was also completely inhibited by [D-Lys] GHRP-6. These results suggest that ghrelin induced the pacemaker potential depolarization through the ghrelin receptor in a G protein-, IP3-, Rho kinase-, and PKC-dependent manner via intracellular and extracellular Ca2+ regulation. In addition, motilin was able to depolarize the pacemaker potentials of ICCs through the ghrelin receptor. Therefore, ghrelin and its receptor may modulate GI motility by acting on ICCs in the murine small intestine.