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DAMGO modulates two-pore domain K+ channels in the substantia gelatinosa neurons of rat spinal cord
PyungSunCho, HanKyuLee, , SangHoonLee, JayZoonIm, SungJunJung 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.5 10 525-531 (7 pages)
The analgesic mechanism of opioids is known to decrease the excitability of substantia gelatinosa (SG) neurons receiving the synaptic inputs from primary nociceptive afferent fiber by increasing inwardly rectifying K+ current. In this study, we examined whether a μ-opioid agonist, [D-Ala2,N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO), affects the two-pore domain K+ channel (K2P) current in rat SG neurons using a slice whole-cell patch clamp technique. Also we confirmed which subtypes of K2P channels... -
Effect of pertussis toxin pretreated centrally on blood glucose level induced by stress
Hong-WonSuh, Yun-BeomSim, Soo-HyunPark, NaveenSharma, Hyun-JuIm, Jae-SeungHong 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.5 4 467-476 (10 pages)
In the present study, we examined the effect of pertussis toxin (PTX) administered centrally in a variety of stress-induced blood glucose level. Mice were exposed to stress after the pretreatment of PTX (0.05 or 0.1 mg) i.c.v. or i.t. once for 6 days. Blood glucose level was measured at 0, 30, 60 and 120 min after stress stimulation. The blood glucose level was increased in all stress groups. The blood glucose level reached at maximum level after 30 min of stress stimulation and returned to a... -
Preventive effects of imperatorin on perfluorohexanesulfonate-induced neuronal apoptosis via inhibition of intracellular calcium-mediated ERK pathway
EunkyungLee, So-YoungChoi, Jae-HoYang, YounJuLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.4 9 399-406 (8 pages)
Early life neuronal exposure to environmental toxicants has been suggested to be an important etiology of neurodegenerative disease development. Perfluorohexanesulfonate (PFHxS), one of the major perfluoroalkyl compounds, is widely distributed environmental contaminants. We have reported that PFHxS induces neuronal apoptosis via ERK-mediated pathway. Imperatorin is a furanocoumarin found in various edible plants and has a wide range of pharmacological effects including neuroprotection. In this... -
Sequestration of sorcin by aberrant forms of tau results in the defective calcium homeostasis
Song-InKim, HeeJaeLee, Sung-SooKim, Yong-SooKwon, WanjooChun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 11 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.4 8 387-397 (11 pages)
Neurofibrillary tangles (NFTs) of microtubule-associated protein tau are a pathological hallmark of Alzheimer’s disease (AD). Endoplasmic reticulum (ER) stress has been known to be involved in the pathogenesis of AD. However, the exact role of ER stress in tau pathology has not yet been clearly elucidated. In present study, the possible relationship between tau pathology and ER stress was examined in terms of sorcin, which is a calcium binding protein and plays an important role in calcium... -
The neuroprotective mechanism of ampicillin in a mouse model of transient forebrain ischemia
Kyung-EonLee, Kyung-OkCho, Yun-SikChoi, SeongYunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2016, Vol.20 No.2 7 185-192 (8 pages)
Ampicillin, a β-lactam antibiotic, dose-dependently protects neurons against ischemic brain injury. The present study was performed to investigate the neuroprotective mechanism of ampicillin in a mouse model of transient global forebrain ischemia. Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral common carotid artery occlusion for 40 min. Before transient forebrain ischemia, ampicillin (200 mg/kg, intraperitoneally [i.p.]) or penicillin G (6,000 U/kg or 20,000 U/kg,... -
Enhancement of GluN2B Subunit-Containing NMDA Receptor Underlies Serotonergic Regulation of Long-Term Potentiation after Critical Period in the Rat Visual Cortex
KayoungJoo, Duck-JooRhie, , Hyun-JongJang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 9 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.6 7 523-531 (9 pages)
Serotonin [5-hydroxytryptamine (5-HT)] regulates synaptic plasticity in the visual cortex. Although the effects of 5-HT on plasticity showed huge diversity depending on the ages of animals and species, it has been unclear how 5-HT can show such diverse effects. In the rat visual cortex, 5-HT suppressed long-term potentiation (LTP) at 5 weeks but enhanced LTP at 8 weeks. We speculated that this difference may originate from differential regulation of neurotransmission by 5-HT between the age... -
Mind Bomb-2 Regulates Hippocampus-dependent Memory Formation and Synaptic Plasticity
SomiKim, TaeHyunKim, Hye-RyeonLee, Young-YunKong, Bong-KiunKaang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.6 6 515-522 (8 pages)
Notch signaling is a key regulator of neuronal fate during embryonic development, but its function in the adult brain is still largely unknown. Mind bomb-2 (Mib2) is an essential positive regulator of the Notch pathway, which acts in the Notch signal-sending cells. Therefore, genetic deletion of Mib2 in the mouse brain might help understand Notch signaling-mediated cell-cell interactions between neurons and their physiological function. Here we show that deletion of Mib2 in the mouse brain... -
Epigallocatechin-3-Gallate (EGCG) Attenuates Traumatic Brain Injury by Inhibition of Edema Formation and Oxidative Stress
BoZhang, BingWang, ShuhuaCao, YongqiangWang 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.6 3 491-497 (7 pages)
Traumatic brain injury (TBI) is a major cause of mortality and long-term disability, which can decrease quality of life. In spite of numerous studies suggesting that Epigallocatechin-3- gallate (EGCG) has been used as a therapeutic agent for a broad range of disorders, the effect of EGCG on TBI remains unknown. In this study, a weight drop model was established to evaluate the therapeutic potential of EGCG on TBI. Rats were administered with 100 mg/kg EGCG or PBS intraperitoneally. At different... -
Dieckol Attenuates Microglia-mediated Neuronal Cell Death via ERK, Akt and NADPH Oxidase-mediated Pathways
YanjiCui, Jee-YunPark, JinjiWu, JiHyungLee, Yoon-SilYang, Moon-SeokKang, Sung-CherlJung, JooMinPark, Eun-SookYoo, Seong-HoKim, SangmeeAhnJ 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.3 5 219-228 (10 pages)
signal-regulated kinase (ERK), Akt and nicotinamide adenine dinuclelotide phosphate (NADPH) oxidase-mediated pathways. In addition, the neuroprotective mechanism of DEK was investigated in microglia-mediated neurotoxicity models such as neuron-microglia co-culture and microglial conditioned media system. Our results demonstrated that treatment of anti-oxidant DEK potently suppressed phosphorylation of ERK in lipopolysaccharide (LPS, 1 μg/ml)-stimulated BV-2 microglia. In addition, DEK markedly... -
Low Non-NMDA Receptor Current Density as Possible Protection Mechanism from Neurotoxicity of Circulating Glutamate on Subfornical Organ Neurons in Rats
WoneeChong, SeongNamKim, SeongKyuHan, SoYeongLee, PanDongRyu 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2015, Vol.19 No.2 13 177-181 (5 pages)
The subfornical organ (SFO) is one of circumventricular organs characterized by the lack of a normal blood brain barrier. The SFO neurons are exposed to circulating glutamate (60∼100 μM), which may cause excitotoxicity in the central nervous system. However, it remains unclear how SFO neurons are protected from excitotoxicity caused by circulating glutamate. In this study, we compared the glutamate-induced whole cell currents in SFO neurons to those in hippocampal CA1 neurons using the patch...


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