The inhibition of long-term potentiation in the rat dentate gyrus by pro-inflammatory cytokines is attenuated in the presence of nicotine

被引:31
作者
Curran, BP [1 ]
O'Connor, JJ [1 ]
机构
[1] Univ Coll Dublin, Conway Inst Biomol & Biomed Res, Dept Human Anat & Physiol, Dublin 2, Ireland
关键词
nicotine; long-term potentiation; interleukin; 1; beta; interleukin-18; tumour necrosis factor-alpha; depotentiation; hippocampus;
D O I
10.1016/S0304-3940(03)00440-3
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Nicotine has previously been shown to affect both long-term potentiation (LTP) and long-term. depression and to reverse age-related impairments of LTP in the hippocampus. Levels of proinflammatory cytokines are known to be elevated with age and to inhibit LTP. In the present study we have investigated the effects of three pro-inflammatory cytokines on nicotine-enhanced LTP in the rat hippocampus in vitro. In the presence of nicotine the inhibitory effect of interleukin-1beta, interleukin-18 and tumour necrosis factor-alpha on LTP was eliminated. Furthermore, significant depotentiation of established LTP could not be obtained in slices treated with nicotine. These experiments demonstrate that nicotine can reverse the inhibitory effects of pro-inflammatory cytokines on LTP. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:103 / 106
页数:4
相关论文
共 22 条
[1]   P42/44 MAP kinase inhibitor PD98059 attenuates multiple forms of synaptic plasticity in rat dentate gyrus in vitro [J].
Coogan, AN ;
O'Leary, DM ;
O'Connor, JJ .
JOURNAL OF NEUROPHYSIOLOGY, 1999, 81 (01) :103-110
[2]  
CUNNINGHAM AJ, 1997, NEUROSCI LETT, V203, P1
[3]   The pro-inflammatory cytokine interleukin-18 impairs long-term potentiation and NMDA receptor-mediated transmission in the rat hippocampus in vitro [J].
Curran, B ;
O'Connor, JJ .
NEUROSCIENCE, 2001, 108 (01) :83-90
[4]   A role for c-Jun N-terminal kinase in the inhibition of long-term potentiation by interleukin-1β and long-term depression in the rat dentate gyrus in vitro [J].
Curran, BP ;
Murray, HJ ;
O'Connor, JJ .
NEUROSCIENCE, 2003, 118 (02) :347-357
[5]   Nicotine activates the extracellular signal-regulated kinase 1/2 via the α7 nicotinic acetylcholine receptor and protein kinase A, in SH-SY5Y cells and hippocampal neurones [J].
Dajas-Bailador, FA ;
Soliakov, L ;
Wonnacott, S .
JOURNAL OF NEUROCHEMISTRY, 2002, 80 (03) :520-530
[6]   β-amyloid activates the mitogen-activated protein kinase cascade via hippocampal α7 nicotinic acetylcholine receptors:: In vitro and in vivo mechanisms related to Alzheimer's disease [J].
Dineley, KT ;
Westerman, M ;
Bui, D ;
Bell, K ;
Ashe, KH ;
Sweatt, JD .
JOURNAL OF NEUROSCIENCE, 2001, 21 (12) :4125-4133
[7]   A requirement for the mitogen-activated protein kinase cascade in hippocampal long term potentiation [J].
English, JD ;
Sweatt, JD .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1997, 272 (31) :19103-19106
[8]   Inactivation of α7 ACh receptors and activation of non-α7 ACh receptors both contribute to long term potentiation induction in the hippocampal CA1 region [J].
Fujii, S ;
Ji, ZX ;
Sumikawa, K .
NEUROSCIENCE LETTERS, 2000, 286 (02) :134-138
[9]   Acute and chronic nicotine exposure differentially facilitate the induction of LTP [J].
Fujii, S ;
Ji, ZX ;
Morita, N ;
Sumikawa, K .
BRAIN RESEARCH, 1999, 846 (01) :137-143
[10]   Nicotine reverses GABAergic inhibition of long-term potentiation induction in the hippocampal CA1 region [J].
Fujii, S ;
Jia, YS ;
Yan, AZ ;
Sumikawa, K .
BRAIN RESEARCH, 2000, 863 (1-2) :259-265