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Developmental Disability Animal Model Based on Neonatal Lipopolysaccharide with Altered 5-HT Function
JaeGooKim, MinSooKim, SeoulLee, GunTaeKim, JongDooLee, DongGooKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.3 6 113-119 (7 pages)
decreased white matter volume and increased serotonergic fibers. The LPS and NAN-190-treated group also exhibited neurologic deficit in the placing reaction test and impaired equilibrium function in the tilt table test. The results showed that a variety of altered behaviors can be generated by two factor model, and suggested that combination of important etiologic factors and possible underlying defects is a promising strategy of establishing an animal model for developmental disabilities. -
A1 Receptor-mediated Protection against Amyloid Beta-induced Injury in Human Neuroglioma Cells
YongWoonCho, HyunJuJung, YongKeunKim, JaeSukWoo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 7 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2007, Vol.11 No.2 1 37-43 (7 pages)
in the central nervous systems as well as myocardium by activating cell surface adenosine receptors. However, the exact target and mechanism of its action still remain controversial. The present study was performed to examine whether adenosine has a protective effect against Aβ-induced injury in neuroglial cells. The astrocyte-derived human neuroglioma cell line, A172 cells, and Aβ25∼35 were employed to produce an experimental Aβ-induced glial cell injury model. Adenosine significantly... -
Involvement of Caspases and Bcl-2 Family in Nitric Oxide-Induced Apoptosis of Rat PC12 Cells
Yeon-JinJeong, Ji-YeonJung, Jin-HaLee, Jin-HyoungCho, Guem-SugLee, Sun-HunKim, Won-JaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.6 6 329-336 (8 pages)
the nitric oxide (NO)-induced cytotoxic mechanism in PC12 cells. Sodium nitroprusside (SNP), an NO donor, decreased the viability of PC12 cells in dose- and time- dependent manners. SNP enhanced the production of reactive oxygen species (ROS), and gave rise to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. Expression of Bax was not affected, whereas Bcl-2 was downregulated in SNP-treated PC12 cells. SNP augmented the release of cytochrome... -
Alpha-Calcitonin Gene-Related Peptide-Null Mice Shows Normal Responses to Various Noxious Stimuli
JonghoLee, RonaldB.Emeson 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.6 5 323-328 (6 pages)
demonstrate that α-CGRP null mice showed no CGRP immunoreactivity from the spinal cord, implying that CGRPs in the mice spinal cord are mainly a-isoforms. However, the nociceptive behaviors of the null mice are not significantly different from the wild type mice in thermal nociceptive behaviors on hotplate, chemical nociception tests to intraplantar capsaicin or formalin injection, and visceral pain behaviors to intraperitoneal acetic acid or magnesium sulfate injections. These data suggest... -
Glycyrrhizin and Morroniside Stimulate Mucin Secretion from Cultured Airway Epithelial Cells
HoJinHeo, HyunJaeLee, CheolsuKim, KunHoSon, YoungChoongKim, YoungSikKim, SamSikKang, YangChunPark, YunHeeKim, UnKyoSeo, JeongHoSeok, Choong 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.6 4 317-322 (6 pages)
we investigated whether glycyrrhizin, prunetin and morroniside affect mucin secretion from cultured airway epithelial cells and compared the possible activities of these agents with the inhibitory action on mucin secretion by poly-L-lysine (PLL) and the stimulatory action by adenosine triphosphate (ATP). Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled using 3H-glucosamine for 24 h and chased for 30 min in the presence of varying concentrations o... -
Calcium Ions are Involved in Modulation of Melittin-induced Nociception in Rat: II. Effect of Calcium Chelator
HongKeeShin, KyungHeeLee, ChulHyunCho 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.6 1 297-302 (6 pages)
which are characteristics similar to those induced by whole bee venom. Melittin-induced nociception has been known to be modulated by the changes in the activity of excitatory amino acid receptors, voltage-dependent calcium channels, cyclooxygenase and serotonin receptors. The present study was undertaken to investigate the role of calcium chelators (TMB-8 & Quin 2) in melittin-induced nociceptive responses. Changes of mechanical threshold and spontaneous flinching behaviors were measured at... -
Involvement of Bcl-2 Family and Caspases Cascade in Sodium Fluoride-Induced Apoptosis of Human Gingival Fibroblasts
Ji-YeonJung, Jae-HongPark, Yeon-JinJeong, Kyu-HoYang, Nam-KiChoi, Sun-HunKim, Won-JaeKim 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 6 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.5 10 289-294 (6 pages)
to apoptotic morphological changes including cell shrinkage, chromatin condensation, and DNA fragmentation. However, NaF did not affect the production of ROS. In addition, NaF augumented cytochrome c release from mitochondria into the cytosol, and enhanced caspase -9 and -3 activities., cleavage (85 kDa fragments) of poly (ADP-ribose) polymerase (PARP) and upregulation of voltage-dependent anion channel (VDAC) 1. These results demonstrated that NaF-induced apoptosis in HGF may be mediated with... -
Calcium Ions are Involved in Modulation of Melittin-induced Nociception in Rat: I. Effect of Voltage-gated Calcium Channel Antagonist
HongKeeShin, KyungHeeLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.5 6 255-262 (8 pages)
C and serotonin receptor. The present study was undertaken to investigate the peripheral and spinal actions of voltage-gated calcium channel antagonists on melittin-induced nociceptive responses. Changes in mechanical threshold and number of flinchings were measured after intraplantar (i.pl.) injection of melittin (30μg/paw) into mid-plantar area of hindpaw. L-type calcium channel antagonists, verapamil [intrathecal (i.t.), 6 or 12μg; i.pl.,100 & 200μg; i.p., 10 or 30 mg], N-type calcium... -
Inhibition of Adenosine Triphosphate-stimulated Mucin Secretion from Airway Epithelial Cells by Schizandrin
HoJinHeo, HyunJaeLee, CheolsuKim, KiHwanBae, YoungSikKim, SamSikKang, YangChunPark, YunHeeKim, UnKyoSeo, JeongHoSeok, ChoongJaeLee 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 4 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.5 5 251-254 (4 pages)
whether schizandrin, schizandrin-A and gomisin-A affect adenosine triphosphate (ATP)-induced mucin secretion from cultured airway epithelial cells. Confluent primary hamster tracheal surface epithelial (HTSE) cells were metabolically radiolabeled using 3H-glucosamine for 24 h and chased for 30 min in the presence of varying concentrations of each agent to assess the effects on 3H-mucin secretion. The results were as follows: 1) schizandrin significantly inhibited ATP-induced mucin secretion; 2)... -
Neurovascular Mechanisms in Stroke, Neurodegeneration and Recovery
EngH.Lo 대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 8 Pages
대한생리학회-대한약리학회 The Korean Journal of Physiology & Pharmacology 2006, Vol.10 No.5 1 223-230 (8 pages)
manifested as cell signaling perturbations at the neurovascular interface. In this mini-review, we will examine 3 examples of this hypothesis: neurovascular mechanisms involved in the thrombolytic therapy of stroke, the crosstalk between neurogenesis and angiogenesis, and the link between vascular dysfunction and amyloid pathology in Alzheimer's disease. An understanding of cell-cell and cell-matrix signaling at the neurovascular interface may yield new approaches for targeting CNS disorders.


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