A role for inflammatory mediators in the IL-18 mediated attenuation of UP in the rat dentate gyrus

被引:39
作者
Cumiskey, D. [1 ]
Curran, B. P. [1 ]
Herron, C. E. [1 ]
O'Connor, J. J. [1 ]
机构
[1] UCD Sch Biomol & Biomed, UCD Conway Inst Biomol & Biomed Res, Dublin 4, Ireland
关键词
interleukin-18; long-term potentiation; PPARy; COX-2; iNOS;
D O I
10.1016/j.neuropharm.2007.03.006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Pro-inflammatory cytokines are known to be elevated in several pathological conditions that are associated with deficits in cognition. We have previously demonstrated that interleukin-18 (IL-18) inhibits long-term potentiation (LTP) in the dentate gyrus in vitro. In this study we have examined the involvement of the inflammatory mediators COX-2 and iNOS in IL-18-mediated inhibition of LTR The effect of an anti-inflammatory PPAR gamma agonist was also investigated. We report that the impairment of UP by IL-18 is significantly attenuated by prior application of the COX-2 inhibitor, SC-236 and the iNOS inhibitor 1400W. These agents had no effect on paired pulse depression in the dentate gyrus. Furthermore, application of the PPAR gamma agonist ciglitazone also attenuated IL-18-mediated inhibition of LTR We discuss a role for p38 MAP kinase in these effects. This study provides novel evidence for the involvement of inflammatory mediators in IL-18-mediated inhibition of LTP in the rat dentate gyrus in vitro. (c) 2007 Elsevier Ltd. All rights reserved.
引用
收藏
页码:1616 / 1623
页数:8
相关论文
共 38 条
[21]   MAP kinase cascades are activated in astrocytes and preadipocytes by 15-deoxy-Δ12-14-prostaglandin J2 and the thiazolidinedione ciglitazone through peroxisome proliferator activator receptor γ-independent mechanisms involving reactive oxygenated species [J].
Lennon, AM ;
Ramaugé, M ;
Dessouroux, A ;
Pierre, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (33) :29681-29685
[22]   Aberrant expression of nNOS in pyramidal neurons in Alzheimer's disease is highly co-localized with p21ras and p16INK4a [J].
Lüth, HJ ;
Holzer, M ;
Gertz, HJ ;
Arendt, T .
BRAIN RESEARCH, 2000, 852 (01) :45-55
[23]   Induction of the proinflammatory cytokine interleukin-18 by axonal injury [J].
Menge, T ;
Jander, S ;
Stoll, G .
JOURNAL OF NEUROSCIENCE RESEARCH, 2001, 65 (04) :332-339
[24]   Macrophage colony-stimulating factor augments β-amyloid-induced interleukin-1, interleukin-6, and nitric oxide production by microglial cells [J].
Murphy, GM ;
Yang, L ;
Cordell, B .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1998, 273 (33) :20967-20971
[25]   A role for COX-2 and p38 mitogen activated protein kinase in long-term depression in the rat dentate gyrus in vitro [J].
Murray, HJ ;
O'Connor, JJ .
NEUROPHARMACOLOGY, 2003, 44 (03) :374-380
[26]   Molecular mechanisms of lipopolysaccharide-induced cyclooxygenase-2 expression in human neutrophils: involvement of the mitogen-activated protein kinase pathway and regulation by anti-inflammatory cytokines [J].
Nagano, S ;
Otsuka, T ;
Niiro, H ;
Yamaoka, K ;
Arinobu, Y ;
Ogami, E ;
Akahoshi, M ;
Inoue, Y ;
Miyake, K ;
Nakashima, H ;
Niho, Y ;
Harada, M .
INTERNATIONAL IMMUNOLOGY, 2002, 14 (07) :733-740
[27]   Cyclooxygenase-2: Molecular biology, pharmacology, and neurobiology [J].
O'Banion, MK .
CRITICAL REVIEWS IN NEUROBIOLOGY, 1999, 13 (01) :45-82
[28]   Group II and III metabotropic glutamate receptors modulate paired pulse depression in the rat dentate gyrus in vitro [J].
O'Leary, DM ;
Cassidy, EM ;
O'Connor, JJ .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1997, 340 (01) :35-44
[29]   IL-4-induced peroxisome proliferator-activated receptor γ activation inhibits NF-κB trans activation in central nervous system (CNS) glial cells and protects oligodendrocyte progenitors under neuroinflammatory disease conditions:: Implication for CNS-demyelinating diseases [J].
Paintlia, Ajaib S. ;
Paintlia, Manjeet K. ;
Singh, Inderjit ;
Singh, Avtar K. .
JOURNAL OF IMMUNOLOGY, 2006, 176 (07) :4385-4398
[30]   Cyclooxygenase-2 expression is increased in frontal cortex of Alzheimer's disease brain [J].
Pasinetti, GM ;
Aisen, PS .
NEUROSCIENCE, 1998, 87 (02) :319-324