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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)
Nitric oxide (NO) has both neuroprotective and neurotoxic effects depending on its concentration and the experimental model. We tested the effects of NG-nitro-L-arginine methyl ester (L-NAME), a nonselective nitric oxide synthase (NOS) inhibitor, and aminoguanidine, a selective inducible NOS (iNOS) inhibitor, on kainic acid (KA)-induced seizures and hippocampal CA3 neuronal death. L-NAME (50 mg/kg, i.p.) and/or aminoguanidine (200 mg/kg, i.p.) were administered 1 h prior to the... -
Water Extract of Samultang Reduces Apoptotic Cell Death by H2O2-Induced Oxidative Injury in SK-N-MC Cells
GyoungWanLee, MinSunKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.3 1 139-145 (7 pages)
significantly reduced apoptotic cell death induced by incubation with 30ՌM H2O2 in SK-N-MC cells. Pre-incubation with water extract of SMT for 2 h prevented the H2O2-induced decrease in mitochondrial transmembrane potential. SMT also attenuated the increase in caspase-3 activity and the breakdown of PARP protein caused by H2O2-induced oxidative stress. These results suggest that the water extract of SMT provides inhibition of apoptotic cell death against oxidative injury in SK-N-MC cells. -
The Effect of Extracellular Glutamate Release on Repetitive Transient Ischemic Injury in Global Ischemia Model
GiJaLee, SeokKeunChoi, YunHyeEo, SungWookKang, SamjinChoi, JeongHoonPark, JiEunLim, KyungWonHong, HyunSeokJin, BermSeokOh, HunKukPark 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 4 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2009, Vol.13 No.1 4 23-26 (4 pages)
resulting in the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this study, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model to compare between single occlusion and repeated transient occlusions within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level... -
Heat Acclimatization in Hot Summer for Ten Weeks Suppress the Sensitivity of Sweating in Response to Iontophoretically-administered Acetylcholine
Jeong-BeomLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.6 10 349-356 (8 pages)
To determine the peripheral mechanisms involved in thermal sweating during the hot summers in July before acclimatization and after acclimatization in September, we evaluated the sweating response of healthy subjects (n=10) to acetylcholine (ACh), a primary neurotransmitter involved in peripheral sudomotor sensitivity. The quantitative sudomotor axon reflex test (QSART) measures sympathetic C fiber function after iontophoresed ACh evokes a measurable reliable sweat response. The QSART, at 2 mA... -
Spinal Metabotropic Glutamate Receptors (mGluRs) are Involved in the Melittin-induced Nociception in Rats
ChulHyunCho, HongKeeShin 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.5 4 237-244 (8 pages)
a sustained decrease of mechanical threshold, spontaneous flinchings and edema. The effects of melittin to reduce mechanical threshold and to induce spontaneous flinchings were significantly suppressed following intrathecal pre-administration of group I mGluR, mGluR1 and mGluR5 antagonists, group II and III mGluR agonists. Group I mGluR antagonists and group II and III mGluR agonists had no significant effect on melittin-induced edema. These experimental findings indicate that multiple spinal... -
Relaxant Effect of Spermidine on Acethylcholine and High K+- induced Gastric Contractions of Guinea-Pig
YoungChulKim, JaeHoonSim, Woong-Choi, ChanHyungKim, Ra-YoungYou, Wen-XieXu, SangJinLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.2 4 59-64 (6 pages)
wide range of test potential in current/voltage (I/V) relationship. Pre- and post-application of spermidine (5 mM) also significantly inhibited carbachol (CCh) and ACh-induced initial and phasic contractions. Finally, caffeine (10 mM)-induced contraction which is activated by Ca2+-induced Ca2+ release (CICR),` was also inhibited by pretreatment of spermidine (5 mM). These findings suggest that spermidine inhibits spontaneous and CCh-induced contraction via inhibition of VDCCL and Ca2+ releasing... -
Roles of Dopaminergic D1 and D2 Receptors in Catecholamine Release from the Rat Adrenal Medulla
YoungJooBaek, YooSeongSeo, DongYoonLim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 12 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2008, Vol.12 No.1 3 13-24 (12 pages)
on the release of catecholamines (CA) evoked by cholinergic stimulation and membrane depolarization from the isolated perfused model of the rat adrenal medulla. SKF81297 (30ՌM) and R-(-)-TNPA (30ՌM) perfused into an adrenal vein for 60 min, produced great inhibition in the CA secretory responses evoked by ACh (5.32×10-3 M), DMPP (10-4 M), McN-A-343 (10-4 M), high K+ (5.6×10-2 M), Bay-K-8644 (10ՌM), and cyclopiazonic acid (10ՌM), respectively. For the release of CA... -
Identification of Differentially Expressed Genes in Murine Hippocampus by Modulation of Nitric Oxide in Kainic Acid-induced Neurotoxic Animal Model
YoAhnSuh, OMinKwon, SoYoungYim, HeeJaeLee, Sung-SooKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.4 3 149-154 (6 pages)
Kainic acid (KA) causes neurodegeneration, but no consensus has been reached concerning its mechanism. Nitric oxide may be a regulator of the mechanism. We identified differentially expressed genes in the hippocampus of mice treated with kainic acid, together with or without L-NAME, a nonselective nitric oxide synthase inhibitor, using a new differential display PCR method based on annealing control primers. Eight genes were identified, including clathrin light polypeptide, TATA element... -
Role of Gap Junction in the Regulation of Renin Release and Intracellular Calcium in As 4.1 Cell Line
JeongHeeHan, Bing-ZheHong, YoungGeunKwak, KuichangYuan, WooHyunPark, SungZooKim, SuhnHeeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.3 5 107-112 (6 pages)
dose-dependent and time- dependent manners. Heptanol and octanol, gap junction blockers, also increased renin release, which were less potent than GA. GA-stimulated renin release was attenuated by pretreatment of the cells with amiloride, nifedipine, ryanodine, and thapsigargin. GA dose-dependently increased intracellular Ca2+ concentration, which was attenuated by nifedipine, nimodipine, ryanodine, and thapsigargin. However, RP-cAMP, chelerythrine, tyrphostin A23, or phenylarsine oxide did not... -
Influence of ω-Conotoxin GVIA, Nifedipine and Cilnidipine on Catecholamine Release in the Rat Adrenal Medulla
Byung-SikYu, Byeong-CheolKim, Dong-YoonLim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 10 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.1 4 21-30 (10 pages)
release evoked by McN-A-343 and cyclopiazonic acid was CNP>NIF>CTX. Also, the rank orders for high K and for DMPP were NIF>CTX>CNP and NIF>CNP>CTX, respectively. Taken together, these results demonstrate that all voltage-dependent Ca2 channels (VDCCs) blockers of cilnidipine, nifedipine, and ω-conotoxin GVIA inhibit greatly the CA release evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization without affecting the basal...


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