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Ionic Mechanisms (ionic + mechanism)
Selected AbstractsIonic Mechanisms and Vectorial Model of Early Repolarization Pattern in the Surface Electrocardiogram of the AthleteANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2008Eduardo C. Barbosa M.D. Background: The electrocardiogram (ECG) of the athlete displays particular characteristics as a consequence of both electrophysiological and autonomic remodeling of the heart that follows continued physical training. However, doubts persist on how these changes directly interact during ventricular activation and repolarization ultimately affecting surface ECG waveforms in athletes. Objective: This article considers an in deep rationale for the electrocardiographic pattern known as early repolarization based on both electrophysiological mechanisms at cellular level and the vectorial theory of the cardiac activation. Methods: The mechanism by which the autonomic remodeling influences the cardiac electrical activation is reviewed and an insight model of the ventricular repolarization based on ionic models and the vectorial theory of the cardiac activation is proposed. Results: Considering the underlying processes related to ventricular electrical remodeling, we propose that, in athletes' heart: 1) vagal modulation increases regional electrophysiological differences in action potential phases 1 and 2 amplitudes, thus enhancing a voltage gradient between epicardial and endocardial fibers; 2) this gradient affects depolarization and repolarization timing sequences; 3) repolarization wave front starts earlier on ventricular wall and partially overcomes the end of depolarization causing an upward displacement of the J-point, ST segment elevation, and inscription of magnified T-waves amplitudes leading to characteristic surface ECG waveform patterns. Conclusions: In athletes, the association between epicardial to endocardial electrophysiological differences and early repolarization ECG pattern can be demonstrated by the vectorial theory of the ventricular activation and repolarization. [source] Muscarine activates the sodium,calcium exchanger via M3 receptors in basal forebrain neuronsEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 8 2006Changqing Xu Abstract Neurons of the medial septum/diagonal band of Broca (MSDB) project to the hippocampus. Muscarinic cholinergic mechanisms within the MSDB are potent modulators of hippocampal functions; intraseptal scopolamine disrupts and intraseptal carbachol facilitates hippocampus-dependent learning and memory tasks, and the associated hippocampal theta rhythm. In earlier work, we demonstrated that, within the MSDB, the septohippocampal GABAergic but not cholinergic neurons are the primary target of muscarinic manipulations and that muscarinic activation of septohippocampal GABAergic neurons is mediated directly via M3 receptors. In the present study, we examined the ionic mechanism(s) underlying the excitatory actions of muscarine in these neurons. Using whole-cell patch-clamp recording techniques in rat brain slices, we demonstrated that M3 receptor-mediated muscarinic activation of MSDB neurons is dependent on external Na+ and is also reduced by bath-applied Ni2+ and KB-R7943 as well as by replacing external Na+ with Li+, suggesting a primary involvement of the Na+,Ca2+ exchanger. We conclude that the M3 receptor-mediated muscarinic activation of MSDB septohippocampal GABA-type neurons, that is important for cognitive functioning, is mediated via activation of the Na+,Ca2+ exchanger. [source] Glucose-induced inhibition: how many ionic mechanisms?ACTA PHYSIOLOGICA, Issue 3 2010D. Burdakov Abstract Sensing of sugar by specialized ,glucose-inhibited' cells helps organisms to counteract swings in their internal energy levels. Evidence from several cell types in both vertebrates and invertebrates suggests that this process involves sugar-induced stimulation of plasma membrane K+ currents. However, the molecular composition and the mechanism of activation of the underlying channel(s) remain controversial. In mouse hypothalamic neurones and neurosecretory cells of the crab Cancer borealis, glucose stimulates K+ currents displaying leak-like properties. Yet knockout of some of the candidate ,leak' channel subunits encoded by the KCNK gene family so far failed to abolish glucose inhibition of hypothalamic cells. Moreover, in other tissues, such as the carotid body, glucose-stimulated K+ channels appear to be not leak-like but voltage-gated, suggesting that glucose-induced inhibition may engage multiple types of K+ channels. Other mechanisms of glucose-induced inhibition, such as hyperpolarization mediated by opening of Cl, channels and depolarization block caused by closure of KATP channels have also been proposed. Here we review known ionic and pharmacological features of glucose-induced inhibition in different cell types, which may help to identify its molecular correlates. [source] Properties of LTD and LTP of retinocollicular synaptic transmission in the developing rat superior colliculusEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 9 2002Fu-Sun Lo Abstract The developing retinocollicular pathway undergoes synaptic refinement in order to form the precise retinotopic pattern seen in adults. To study the mechanisms which underlie refinement, we investigated long-term changes in retinocollicular transmission in rats aged P0,P25. Field potentials (FPs) in the superior colliculus (SC) were evoked by stimulation of optic tract fibers in an in vitro isolated brainstem preparation. High intensity stimulation induced long-term depression (LTD) in the SC after both low (1000 stimuli at 1 Hz) and higher (1000 stimuli at 50 Hz) frequency stimulation. The induction of LTD was independent of activation of NMDA and GABAA receptors, because d -APV (100 µM) and bicuculline (10 µM) did not block LTD. Induction of LTD was dependent upon activation of l -type Ca2+ channels as 10 µM nitrendipine, an l -type Ca2+ channel blocker, significantly decreased the magnitude of LTD. LTD was down-regulated during development. LTD magnitude was greatest in rats aged P0,P9 and significantly less in rats aged P10,P25. Long-term potentiation (LTP) was induced by low intensity stimulation and only after high frequency tetanus (1000 stimuli at 50 Hz). LTP was NMDA receptor dependent because d -APV (100 ,M) completely abolished it. LTP induction was also blocked by the l -type Ca2+ channel blocker nitrendipine. The magnitude of LTP first increased with age, being significantly greater at P7,P13 than at P0,3 and then decreased at P23,25. In summary, both LTD and LTP are present during retinocollicular pathway refinement, but have different transmitter and ionic mechanisms and time courses of expression. [source] Flavonoids from Chinese Viscum coloratum: antiarrhythmic efficacy and ionic mechanismsPHYTOTHERAPY RESEARCH, Issue 12 2006Chu Wen-Feng Abstract Viscum coloratum flavonoids (VCF) have been demonstrated to produce a variety of biological actions. An accumulating line of evidence supported the view that VCF may exert protective effects on the cardiovascular system. The aim of the study was to assess the antiarrhythmic activity as well as the electrophysiological properties of VCF. The antiarrhythmic effects of VCF were observed in a rat model of arrhythmia induced by aconitine. VCF significantly and dose-dependently increased the dosage of aconitine required to induce the arrhythmia indexes. Electrophysiological experiment revealed that VCF shortened APD through inhibition of ICa-L. Copyright © 2006 John Wiley & Sons, Ltd. [source] A modelling study of locomotion-induced hyperpolarization of voltage threshold in cat lumbar motoneuronesTHE JOURNAL OF PHYSIOLOGY, Issue 2 2002Yue Dai During fictive locomotion the excitability of adult cat lumbar motoneurones is increased by a reduction (a mean hyperpolarization of ,6.0 mV) of voltage threshold (Vth) for action potential (AP) initiation that is accompanied by only small changes in AP height and width. Further examination of the experimental data in the present study confirms that Vth lowering is present to a similar degree in both the hyperpolarized and depolarized portions of the locomotor step cycle. This indicates that Vth reduction is a modulation of motoneurone membrane currents throughout the locomotor state rather than being related to the phasic synaptic input within the locomotor cycle. Potential ionic mechanisms of this locomotor-state-dependent increase in excitability were examined using three five-compartment models of the motoneurone innervating slow, fast fatigue resistant and fast fatigable muscle fibres. Passive and active membrane conductances were set to produce input resistance, rheobase, afterhyperpolarization (AHP) and membrane time constant values similar to those measured in adult cat motoneurones in non-locomoting conditions. The parameters of 10 membrane conductances were then individually altered in an attempt to replicate the hyperpolarization of Vth that occurs in decerebrate cats during fictive locomotion. The goal was to find conductance changes that could produce a greater than 3 mV hyperpolarization of Vth with only small changes in AP height (< 3 mV) and width (< 1.2 ms). Vth reduction without large changes in AP shape could be produced either by increasing fast sodium current or by reducing delayed rectifier potassium current. The most effective Vth reductions were achieved by either increasing the conductance of fast sodium channels or by hyperpolarizing the voltage dependency of their activation. These changes were particularly effective when localized to the initial segment. Reducing the conductance of delayed rectifier channels or depolarizing their activation produced similar but smaller changes in Vth. Changes in current underlying the AHP, the persistent Na+ current, three Ca2+ currents, the ,h' mixed cation current, the ,A' potassium current and the leak current were either ineffective in reducing Vth or also produced gross changes in the AP. It is suggested that the increased excitability of motoneurones during locomotion could be readily accomplished by hyperpolarizing the voltage dependency of fast sodium channels in the axon hillock by a hitherto unknown neuromodulatory action. [source] ELECTROPHYSIOLOGICAL EFFECTS OF KETAMINE ON HUMAN ATRIAL MYOCYTES AT THERAPEUTICALLY RELEVANT CONCENTRATIONSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 12 2008Chun-Yu Deng SUMMARY 1Ketamine is widely used for the induction of anaesthesia in high-risk patients with cardiovascular instability or severe hypovolaemia. However, the ionic mechanisms involved in the effects of ketamine at therapeutically relevant concentrations in human cardiac myocytes are unclear. The present study was designed to investigate the effects of ketamine on L-type Ca2+ (ICa), transient outward K+ (Ito), ultra-rapid delayed rectifier K+ (IKur) and inward rectifier potassium (IK1) currents, as well as on action potentials, in human isolated atrial myocytes. 2Atrial myocytes were isolated enzymatically from specimens of human atrial appendage obtained from patients undergoing coronary artery bypass grafting. The action potential and membrane currents were recorded in both current- and voltage-clamp modes using the patch-clamp technique. 3Ketamine inhibited ICa with an IC50 of 1.8 µmol/L. In addition, 10 µmol/L ketamine decreased the ICa peak current at +10 mV from 5.1 ± 0.3 to 2.1 ± 0.4 pA/pF (P < 0.01), but did not change the threshold potential, peak current potential and reverse potential. 4Ketamine had no effect on Ito, IKur or IK1, but it reversibly shortened the duration of the action potential in human atrial myocytes. 5In conclusion, ketamine, at a clinically relevant concentration, shortens the action potential duration of the human atrial myocytes, probably by inhibiting ICa. [source] | |||||||||||||