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Rectifying K+ Current (rectifying + k+_current)
Selected AbstractsAndrogen modulates the kinetics of the delayed rectifying K+ current in the electric organ of a weakly electric fishDEVELOPMENTAL NEUROBIOLOGY, Issue 12 2007M. Lynne McAnelly Abstract Weakly electric fish such as Sternopygus macrurus utilize a unique signal production system, the electric organ (EO), to navigate within their environment and to communicate with conspecifics. The electric organ discharge (EOD) generated by the Sternopygus electric organ is quasi-sinusoidal and sexually dimorphic; sexually mature males produce long duration EOD pulses at low frequencies, whereas mature females produce short duration EOD pulses at high frequencies. EOD frequency is set by a medullary pacemaker nucleus, while EOD pulse duration is determined by the kinetics of Na+ and K+ currents in the electric organ. The inactivation of the Na+ current and the activation of the delayed rectifying K+ current of the electric organ covary with EOD frequency such that the kinetics of both currents are faster in fish with high (female) EOD frequency than those with low (male) EOD frequencies. Dihydrotestosterone (DHT) implants masculinize the EOD centrally by decreasing frequency at the pacemaker nucleus (PMN). DHT also acts at the electric organ, broadening the EO pulse, which is at least partly due to a slowing of the inactivation kinetics of the Na+ current. Here, we show that chronic DHT treatment also slows the activation and deactivation kinetics of the electric organ's delayed rectifying K+ current. Thus, androgens coregulate the time-varying kinetics of two distinct ion currents in the EO to shape a sexually dimorphic communication signal. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source] Electrophysiological and morphological characterization of dentate astrocytes in the hippocampusDEVELOPMENTAL NEUROBIOLOGY, Issue 2 2005Masako Isokawa Abstract We studied electrophysiological and morphological properties of astrocytes in the dentate gyrus of the rat hippocampus in slices. Intracellular application of Lucifer yellow revealed two types of morphology: one with a long process extruding from the cell body, and the other with numerous short processes surrounding the cell body. Their electrophysiological properties were either passive, that is, no detectable voltage-dependent conductance, or complex, with Na+/K+ currents similar to those reported in the Ammon's horn astrocytes. We did not find any morphological correlate to the types of electrophysiological profile or dye coupling. Chelation of cytoplasmic calcium ([Ca2+]i) by BAPTA increased the incidence of detecting a low Na+ conductance and transient outward K+ currents. However, an inwardly rectifying K+ current (Kir), a hallmark of differentiated CA1/3 astrocytes, was not a representative K+ -current in the complex dentate astrocytes, suggesting that these astrocytes could retain an immature form of K-currents. Dentate astrocytes may possess a distinct current profile that is different from those in CA1/3 Ammon's horn. © 2005 Wiley Periodicals, Inc. J Neurobiol, 2005 [source] Temperature-sensitive TREK currents contribute to setting the resting membrane potential in embryonic atrial myocytesTHE JOURNAL OF PHYSIOLOGY, Issue 15 2008Hengtao Zhang TREK channels belong to the superfamily of two-pore-domain K+ channels and are activated by membrane stretch, arachidonic acid, volatile anaesthetics and heat. TREK-1 is highly expressed in the atrium of the adult heart. In this study, we investigated the role of TREK-1 and TREK-2 channels in regulating the resting membrane potential (RMP) of isolated chicken embryonic cardiac myocytes. At room temperature, the average RMP of embryonic day (ED) 11 atrial myocytes was ,22 ± 2 mV. Raising the temperature to 35°C hyperpolarized the membrane to ,69 ± 2 mV and activated a large outwardly rectifying K+ current that was relatively insensitive to conventional K+ channel inhibitors (TEA, 4-AP and Ba2+) but completely inhibited by tetracaine (200 ,m), an inhibitor of TREK channels. The heat-induced hyperpolarization was mimicked by 10 ,m arachidonic acid, an agonist of TREK channels. There was little or no inwardly rectifying K+ current (IK1) in the ED11 atrial cells. In marked contrast, ED11 ventricular myocytes exhibited a normal RMP (,86.1 ± 3.4 mV) and substantial IK1, but no temperature- or tetracaine-sensitive K+ currents. Both RT-PCR and real-time PCR further demonstrated that TREK-1 and TREK-2 are highly and almost equally expressed in ED11 atrium but much less expressed in ED11 ventricle. In addition, immunofluorescence demonstrated TREK-1 protein in the membrane of atrial myocytes. These data indicate the presence and function of TREK-1 and TREK-2 in the embryonic atrium. Moreover, we demonstrate that TREK-like currents have an essential role in determining membrane potential in embryonic atrial myocytes, where IK1 is absent. [source] Electrophysiological Effects of the Anti-Cancer Drug Lapatinib on Cardiac RepolarizationBASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 1 2010Hyang-Ae Lee Although lapatinib is associated with a risk of QT prolongation, the effects of the drug on cellular cardiac electrical properties and on action potential duration (APD) have not been studied. To evaluate the potential effects of lapatinib on cardiac repolarization, we investigated its electrophysiological effects using a whole-cell patch,clamp technique in transiently transfected HEK293 cells expressing human ether-à-go-go (hERG; to examine the rapidly activating delayed rectifier K+ current, IKr), KCNQ1/KCNE1 (to examine the slowly activating delayed rectifier K+ current, IKs), KCNJ2 (to examine the inwardly rectifying K+ current, IK1), or SCN5A (to examine the inward Na+ current, INa) and in rat cardiac myocytes (to examine the inward Ca2+ current, ICa). We also examined its effects on the APD at 90% (APD90) in isolated rabbit Purkinje fibres. In ion channel studies, lapatinib inhibited the hERG current in a concentration-dependent manner, with a half-maximum inhibition concentration (IC50) of 0.8 ± 0.09 ,m. In contrast, at concentrations up to 3 ,m, lapatinib did not significantly reduce the INa, IK1 or ICa amplitudes; at 3 ,m, it did slightly inhibit the IKs amplitude (by 19.4 ± 4.7%; p < 0.05). At 5 ,m, lapatinib induced prolongation of APD90 by 16.1% (p < 0.05). These results suggest that the APD90 -prolonging effect of lapatinib on rabbit Purkinje fibres is primarily a result of inhibition of the hERG current and IKs, but not INa, IK1 or ICa. [source] Effects of endomorphin on substantia gelatinosa neurons in rat spinal cord slicesBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2003Su-Ying Wu Whole-cell patch recordings were made from substantia gelatinosa (SG) neurons in transverse lumbar spinal cord slices of 15- to 30-day-old rats. Endomorphin 1 (EM-1) or EM-2 (10 ,M) hyperpolarized or induced an outward current in 26 of the 66 SG neurons. The I,V relationship showed that the peptide activates an inwardly rectifying K+ current. EM-1 or EM-2 (0.3,10 ,M) suppressed short-latency excitatory postsynaptic currents (EPSCs) and long-latency inhibitory postsynaptic currents (IPSCs) in nearly all SG neurons tested or short-latency IPSCs in six of the 10 SG neurons. [Met5] enkephalin or [D -Ala2, N -Me-Phe4, Gly5 -ol]-enkephalin (DAMGO) (1,10 ,M) depressed EPSCs and IPSCs. EM-1 or EM-2 depressed synaptic responses without causing a significant change in holding currents or inward currents induced by glutamate. Glutamate also evoked a short-latency outward current in five SG neurons or a biphasic current in two neurons; the outward current was blocked by tetrodotoxin (TTX, 0.3 ,M) or bicuculline (10 ,M). EM-1 or DAMGO (1 or 5 ,M) attenuated the glutamate-evoked outward or biphasic currents in four of the seven SG neurons. EM-1 (1 ,M) reduced the frequency, but not the amplitude of miniature EPSCs or miniature IPSCs. Naloxone (1 ,M) or the selective , -opioid receptor antagonist , -funaltrexamine (, -FNA, 25 ,M) antagonized the action of EM; EM-induced hyperpolarizations persisted in the presence of the , -opioid receptor antagonist (nor-binaltorphimine dihydrochloride, 1 ,M) and/or , -opioid receptor antagonist (naltrindole hydrochloride, 1 ,M). It may be concluded that EM acting on , -opioid receptors hyperpolarizes a population of SG neurons by activating an inwardly rectifying K+ current, and attenuates excitatory and inhibitory synaptic currents evoked in a population of SG neurons, probably by a presynaptic site of action. British Journal of Pharmacology (2003) 140, 1088,1096. doi:10.1038/sj.bjp.0705534 [source] | |||||||||||||