Tale of tail current

Kodirov, Sodikdjon A.

doi:10.1016/j.pbiomolbio.2019.06.002

Cited by 12 publications

(8 citation statements)

References 164 publications

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“…Earlier investigations have demonstrated a time-dependent change in I K(erg) activation during the envelope-of-tail test [ 21 , 22 , 23 , 24 , 52 ]. Here, we then analyzed an inward activating and deactivating I K(erg) evoked by varying durations of conditioning pulse (from 4 to 2048 ms with a geometrics-based progression) to −10 mV from −110 mV, and the relationship of the relative amplitude versus the pulse duration was established in Figure 5 C. Like earlier investigations [ 21 , 24 ], the envelope-of-tail test tailored for the activation of I K(erg) seen in Neuro-2a cells exhibits a time-dependent exponential decay in the ratio of the relative amplitude (i.e., I act / I deact ) evoked during the pulse durations between 4 and 2048 ms in a geometrics-based progression.…”

Section: Resultsmentioning

confidence: 99%

“…By comparison, the decaying rate of I Na during such high PT stimulation was noticeably faster than that of I K(erg) , I K(M) , or I K(DR) ( Figure 4 , Figure 7 , and Figure 9 ) seen in Neuro-2a cells. Although the gating kinetics or inactivation-dependent mechanisms residing in these K + currents are overly distinguishable [ 21 , 24 , 31 , 46 , 52 ], the difference in current decaying during PT stimulation could be of particular significance. The main reason for this is because the magnitude of these K + currents (i.e., resurgent K + tail currents) could maintain the membrane in a spike-ready state, thus conferring optimal repriming of I Na during the occurrence of prolonged repetitive activity [ 27 , 31 ].…”

Section: Discussionmentioning

confidence: 99%

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Effective Perturbations by Phenobarbital on INa, IK(erg), IK(M) and IK(DR) during Pulse Train Stimulation in Neuroblastoma Neuro-2a Cells

Lai

Cho

et al. 2022

Biomedicines

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Phenobarbital (PHB, Luminal Sodium®) is a medication of the barbiturate and has long been recognized to be an anticonvulsant and a hypnotic because it can facilitate synaptic inhibition in the central nervous system through acting on the γ-aminobutyric acid (GABA) type A (GABAA) receptors. However, to what extent PHB could directly perturb the magnitude and gating of different plasmalemmal ionic currents is not thoroughly explored. In neuroblastoma Neuro-2a cells, we found that PHB effectively suppressed the magnitude of voltage-gated Na+ current (INa) in a concentration-dependent fashion, with an effective IC50 value of 83 µM. The cumulative inhibition of INa, evoked by pulse train stimulation, was enhanced by PHB. However, tefluthrin, an activator of INa, could attenuate PHB-induced reduction in the decaying time constant of INa inhibition evoked by pulse train stimuli. In addition, the erg (ether-à-go-go-related gene)-mediated K+ current (IK(erg)) was also blocked by PHB. The PHB-mediated inhibition on IK(erg) could not be overcome by flumazenil (GABA antagonist) or chlorotoxin (chloride channel blocker). The PHB reduced the recovery of IK(erg) by a two-step voltage protocol with a geometrics-based progression, but it increased the decaying rate of IK(erg), evoked by the envelope-of-tail method. About the M-type K+ currents (IK(M)), PHB caused a reduction of its amplitude, which could not be counteracted by flumazenil or chlorotoxin, and PHB could enhance its cumulative inhibition during pulse train stimulation. Moreover, the magnitude of delayed-rectifier K+ current (IK(DR)) was inhibited by PHB, while the cumulative inhibition of IK(DR) during 10 s of repetitive stimulation was enhanced. Multiple ionic currents during pulse train stimulation were subject to PHB, and neither GABA antagonist nor chloride channel blocker could counteract these PHB-induced reductions. It suggests that these actions might conceivably participate in different functional activities of excitable cells and be independent of GABAA receptors.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Effective Perturbations by Phenobarbital on INa, IK(erg), IK(M) and IK(DR) during Pulse Train Stimulation in Neuroblastoma Neuro-2a Cells

Lai

Cho

et al. 2022

Biomedicines

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“…The same is true even if the Shal in contrast to Shab and Shaw are readily activated from more hyperpolarized HP. Earlier studies used the reversal potential ( E rev ) of K currents as a HP to activate the Kv and Nav channels (Frankenhaeuser, 1962; Kodirov, 2020). Besides, all Kv channels exhibit more specific HP dependencies, and are separated using different and adequate values in the same cells sequentially (Kodirov et al, 2022).…”

Section: K Currents In Drosophilamentioning

confidence: 99%

Functioning of K channels during sleep

Kodirov

2022

Arch Insect Biochem Physiol

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The functioning of voltage-dependent K channels (Kv) may correlate with the physiological state of brain in organisms, including the sleep in Drosophila. Apparently, all major types of K currents are expressed in CNS of this model organism. These are the Shab-Kv2, Shaker-Kv1, Shal-Kv4, and Shaw-Kv3 α subunits and can be deciphered by patch-clamp technique. Although it is plausible that some of these channels may play a prevailing role in sleep or wakefulness, several of recent data are not conclusive. It needs to be defined that indeed the frequency of action potentials in large ventral lateral pacemaker neurons is either higher or lower during the morning or night because of an increased Kv3 and Kv4 currents, respectively. The outcomes of dynamic-clamp approach in combination with electrophysiology in insects are unreliable in contrast to those in mammalian neurons. Since the addition of virtual Kv conductance during any Zeitgeber time should not significantly alter the resting membrane potential. This review explains the Drosophila sleep behavior based on neural activity with respect to K current-driven action potential rate.

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“… 158 Kv11.1 channels exhibit longer‐lasting and higher‐amplitude tail currents than have been found for other outward current channels that contribute to cardiac AP repolarization and duration. 159 …”

Section: Ventricular Ap‐related Ion Channels: Classification Structure Function Regulation and Disease Relevancementioning

confidence: 99%

“…158 Kv11.1 channels exhibit longer-lasting and higheramplitude tail currents than have been found for other outward current channels that contribute to cardiac AP repolarization and duration. 159 Kv11.1 is composed of one pore-forming α subunit and two β subunits (MinK and MiRP1 encoded by KCNE1 and KCNE2) (Figure 4F). The structure of the hERG channel with depolarized voltage sensors and open pores was revealed using cryo-EM.…”

Section: Ta B L Ementioning

confidence: 99%

Ventricular voltage‐gated ion channels: Detection, characteristics, mechanisms, and drug safety evaluation

Chen

Wang

et al. 2021

Clinical & Translational Med

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Cardiac voltage‐gated ion channels (VGICs) play critical roles in mediating cardiac electrophysiological signals, such as action potentials, to maintain normal heart excitability and contraction. Inherited or acquired alterations in the structure, expression, or function of VGICs, as well as VGIC‐related side effects of pharmaceutical drug delivery can result in abnormal cellular electrophysiological processes that induce life‐threatening cardiac arrhythmias or even sudden cardiac death. Hence, to reduce possible heart‐related risks, VGICs must be acknowledged as important targets in drug discovery and safety studies related to cardiac disease. In this review, we first summarize the development and application of electrophysiological techniques that are employed in cardiac VGIC studies alone or in combination with other techniques such as cryoelectron microscopy, optical imaging and optogenetics. Subsequently, we describe the characteristics, structure, mechanisms, and functions of various well‐studied VGICs in ventricular myocytes and analyze their roles in and contributions to both physiological cardiac excitability and inherited cardiac diseases. Finally, we address the implications of the structure and function of ventricular VGICs for drug safety evaluation. In summary, multidisciplinary studies on VGICs help researchers discover potential targets of VGICs and novel VGICs in heart, enrich their knowledge of the properties and functions, determine the operation mechanisms of pathological VGICs, and introduce groundbreaking trends in drug therapy strategies, and drug safety evaluation.

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Tale of tail current

Cited by 12 publications

References 164 publications

Effective Perturbations by Phenobarbital on INa, IK(erg), IK(M) and IK(DR) during Pulse Train Stimulation in Neuroblastoma Neuro-2a Cells

Effective Perturbations by Phenobarbital on INa, IK(erg), IK(M) and IK(DR) during Pulse Train Stimulation in Neuroblastoma Neuro-2a Cells

Functioning of K channels during sleep

Ventricular voltage‐gated ion channels: Detection, characteristics, mechanisms, and drug safety evaluation

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