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양윤실,전상찬,김동관,은수용,정성철 대한약리학회 2017 The Korean Journal of Physiology & Pharmacology Vol.21 No.2
Excessive influx and the subsequent rapid cytosolic elevation of Ca2+ in neurons is the major cause to induce hyperexcitability and irreversible cell damage although it is an essential ion for cellular signalings. Therefore, most neurons exhibit several cellular mechanisms to homeostatically regulate cytosolic Ca2+ level in normal as well as pathological conditions. Delayed rectifier K+ channels (IDR channels) play a role to suppress membrane excitability by inducing K+ outflow in various conditions, indicating their potential role in preventing pathogenic conditions and cell damage under Ca2+-mediated excitotoxic conditions. In the present study, we electrophysiologically evaluated the response of IDR channels to hyperexcitable conditions induced by high Ca2+ pretreatment (3.6 mM, for 24 hours) in cultured hippocampal neurons. In results, high Ca2+-treatment significantly increased the amplitude of IDR without changes of gating kinetics. Nimodipine but not APV blocked Ca2+-induced IDR enhancement, confirming that the change of IDR might be targeted by Ca2+ influx through voltage-dependent Ca2+ channels (VDCCs) rather than NMDA receptors (NMDARs). The VDCC-mediated IDR enhancement was not affected by either Ca2+-induced Ca2+ release (CICR) or small conductance Ca2+-activated K+ channels (SK channels). Furthermore, PP2 but not H89 completely abolished IDR enhancement under high Ca2+ condition, indicating that the activation of Src family tyrosine kinases (SFKs) is required for Ca2+-mediated IDR enhancement. Thus, SFKs may be sensitive to excessive Ca2+ influx through VDCCs and enhance IDR to activate a neuroprotective mechanism against Ca2+-mediated hyperexcitability in neurons.
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이지형,Khulan Amarsanaa,우진지,전상찬,추연지,정성철,박덕배,김세재,한상헌,김현욱,류임주,은수용 대한약리학회 2018 The Korean Journal of Physiology & Pharmacology Vol.22 No.3
Mitochondrial calcium overload is a crucial event in determining the fate of neuronal cell survival and death, implicated in pathogenesis of neurodegenerative diseases. One of the driving forces of calcium influx into mitochondria is mitochondria membrane potential (ΔΨm). Therefore, pharmacological manipulation of ΔΨm can be a promising strategy to prevent neuronal cell death against brain insults. Based on these issues, we investigated here whether nobiletin, a Citrus polymethoxylated flavone, prevents neurotoxic neuronal calcium overload and cell death via regulating basal ΔΨm against neuronal insult in primary cortical neurons and pure brain mitochondria isolated from rat cortices. Results demonstrated that nobiletin treatment significantly increased cell viability against glutamate toxicity (100 μM, 20 min) in primary cortical neurons. Real-time imaging-based fluorometry data reveal that nobiletin evokes partial mitochondrial depolarization in these neurons. Nobiletin markedly attenuated mitochondrial calcium overload and reactive oxygen species (ROS) generation in glutamate (100 μM)-stimulated cortical neurons and isolated pure mitochondria exposed to high concentration of Ca2+ (5 μM). Nobiletininduced partial mitochondrial depolarization in intact neurons was confirmed in isolated brain mitochondria using a fluorescence microplate reader. Nobiletin effects on basal ΔΨm were completely abolished in K+-free medium on pure isolated mitochondria. Taken together, results demonstrate that K+ influx into mitochondria is critically involved in partial mitochondrial depolarization–related neuroprotective effect of nobiletin. Nobiletin-induced mitochondrial K+ influx is probably mediated, at least in part, by activation of mitochondrial K+ channels. However, further detailed studies should be conducted to determine exact molecular targets of nobiletin in mitochondria.
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