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Bark Constituents from Mushroom-detoxified Rhus verniciflua Suppress Kainic Acid-induced Neuronal Cell Death in Mouse Hippocampus
Jong-SeonByun, YoonHeeHan, Sung-JunHong, Sung-MiHwang, Yong-SooKwon, HeeJaeLee, Sung-SooKim, Myong-JoKim, WanjooChun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 5 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.5 5 279-283 (5 pages)
a mouse model of kainic acid (KA)-induced excitotoxicity. KA resulted in significant apoptotic neuronal cell death in the CA3 region of mouse hippocampus. However, seven daily administrations of RVH-1 or RVH-2 prior to KA injection significantly attenuated KA-induced pyramidal neuronal cell death in the CA3 region. Furthermore, pretreatment with RVH-1 and RVH-2 also suppressed KA-induced microglial activation in the mouse hippocampus. The present study demonstrates that RVH-1 and RVH-2 isolated... -
Neuroprotective Effect of Visnagin on Kainic Acid-induced Neuronal Cell Death in the Mice Hippocampus
Min-SooKwon, Jin-KooLee, Soo-HyunPark, Yun-BeomSim, Jun-SubJung, Moo-HoWon, Seon-MiKim, Hong-WonSuh 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.5 2 257-263 (7 pages)
contraction by inhibition of calcium influx into blood cells. However, the neuroprotective effect of visnagin was not clearly known until now. Thus, we investigated whether visnagin has a neuroprotective effect against kainic acid (KA)-induced neuronal cell death. In the cresyl violet staining, pre-treatment or post-treatment visnagin (100 mg/kg, p.o. or i.p.) showed a neuroprotective effect on KA (0.1Ռg) toxicity. KA-induced gliosis and proinflammatory marker (IL-1Ղ, TNF-Ձ,... -
Changes in Endothelin Receptor Type B and Neuronal Nitric Oxide Synthase in Puromycin Aminonucleoside-Induced Nephrotic Syndrome
EunHuiBae, SooWanKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2010, Vol.14 No.4 4 223-228 (6 pages)
(ETBR) was unchanged. The expression of neuronal NOS (nNOS) was decreased in the inner medulla. On day 14, urinary sodium excretion was unchanged compared with controls. The expression of ETBR increased, while nNOS expression in the inner medulla was comparable to controls. These findings suggest that decreased nNOS plays a role in the development of sodium retention in the nephrotic syndrome. Recovery of nNOS and increased renal ETBR synthesis may promote sodium excretion in later stages of the... -
Kainic Acid-induced Neuronal Death is Attenuated by Aminoguanidine but Aggravated by L-NAME in Mouse Hippocampus
Jong-SeonByun, Sang-HyunLee, Seong-HoJeon, Yong-SooKwon, HeeJaeLee, Sung-SooKim, Young-MyeongKim, Myong-JoKim, WanjooChun 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.4 1 265-271 (7 pages)
death with concomitant decreases in iNOS expression and microglial activation. The protective effect of aminoguanidine was maintained for up to 2 weeks. Furthermore, iNOS knockout mice (iNOS−/−) were resistant to KA-induced neuronal death. The present study demonstrates that aminoguanidine attenuates KA-induced neuronal death, whereas L-NAME aggravates neuronal death, in the CA3 region of the hippocampus, suggesting that NOS isoforms play different roles in KA-induced excitotoxicity. -
Pre-ischemic Treatment with Ampicillin Reduces Neuronal Damage in the Mouse Hippocampus and Neostriatum after Transient Forebrain Ischemia
Kyung-EonLee, Seul-KiKim, Kyung-OkCho, SeongYunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.6 1 287-292 (6 pages)
a crucial role in protecting neurons against glutamate excitotoxicity. We investigated the effect of ampicillin on neuronal damage in the mouse hippocampus and neostriatum following transient global forebrain ischemia. Male C57BL/6 mice were anesthetized with halothane and subjected to bilateral occlusion of the common carotid artery for 40 min. Ampicillin was administered post-ischemically (for 3 days) and/or pre-ischemically (for 3∼5 days until one day before the onset of ischemia). Pre- and... -
Involvement of Endoplasmic Reticulum Stress Response in the Neuronal Differentiation
YoonMiCho, YoonSeongJang, Young-MinJang, Jin-YoungSeo, HoShikKim, JeongHwaLee, SeongWhanJeong, InKyungKim, Oh-JooKwon 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.6 2 239-248 (10 pages)
days, early stem cell marker, nestin, expression was decreased from day 4, and neuronal markers such as neurofilament-L, -M and Tuj1 were increased after day 4. In this condition, expressions of BIP, ATF6, and phosphorylated PERK as well as their down stream signaling molecules such as CHOP, ATF4, XBP1, GADD34, Nrf2 and p58IPK were significantly increased, suggesting the induction of ERSR during neuronal differentiation of rCPC. ERSR was also induced during the differentiation of PC12 cells for... -
Baicalein Protects 6-OHDA-induced Neuronal Damage by Suppressing Oxidative Stress
Heh-InIm, EunjooNam, Eun-sunLee, Yu-jinHwang, YongSikKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.6 3 309-316 (8 pages)
The protective effects of baicalein, one of the flavonoids in Scutellaria baicalensis Georgi, were evaluated against 6-hydroxydopamine (6-OHDA)-induced neuronal damage in mice and cultured human neuroblastoma cells. Nigrostriatal damage was induced by stereotaxically injecting 6-OHDA into the right striatum. Baicalein was administered intraperitoneally 30 min before and 90 min after lesion induction. Animals received a further daily injection of baicalein for 3 consecutive days. Two weeks after... -
Effects of Ethosuximide on the Pilocarpine Induced Seizure in Rat Model of Neuronal Migration Disorder
Byung-KonKim, In-SunChoi, Jin-HwaCho, Il-SungJang, Maan-GeeLeeByung-JuChoi 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.5 3 235-242 (8 pages)
Cortical malformation-associated epileptic seizures are resistant to conventional anticonvulsant drugs. Relatively little research has been conducted on the effects of antiepileptic drugs (AEDs) on seizure activity in a rat model of dysplasia. We have used rats exposed to methylazoxymethanol acetate (MAM) in utero, an animal model featuring nodular heterotopia, to investigate the effects of ethosuximide (ETX) in the dysplastic brain. Pilocarpine was used to induce acute seizure in MAM-exposed... -
Inhibition of Nitric Oxide-induced Neuronal Apoptosis in PC12 Cells by Epigallocatechin Gallate
JiYeonJung, YeonJinJeong, ChangRyoungHan, SunHunKim, HyunJinKim, KiHeonLee, HaOkPark, WonJaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.4 8 239-246 (8 pages)
a major compound of green tea, is recognized as protective substance against neuronal diseases. This study is aimed to investigate the effect of EGCG on NO-induced cell death in PC12 cells. Administration of sodium nitroprusside (SNP), a NO donor, decreased cell viability in a dose- and time-dependent manner and induced genomic DNA fragmentation with cell shrinkage and chromatin condensation. EGCG diminished the decrement of cell viability and the formation of apoptotic morphologenic changes as... -
Effects of a δ-opioid Agonist on the Brainstem Vestibular Nuclear Neuronal Activity of Rats
Tae-SunKim, MeiHuang, Myung-JooJang, Han-SeongJeong, Jong-SeongPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2005, Vol.9 No.3 1 137-142 (6 pages)
patch-clamp techniques. The spontaneous action potentials were increased by DADLE in 12 cells and decreased in 3 cells. The spike frequency and resting membrane potential of these cells were increased by DADLE. The depth of afterhyperpolarization was not affected by DADLE. The potassium currents were decreased in 20 cells and increased in 5 cells. These results suggest that DADLE increases the neuronal activity of the medial vestibular nuclear neurons by altering resting membrane potential.


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