The mechanisms of action of commonly used antiepileptic drugs

被引:236
作者
Kwan, P [1 ]
Sills, GJ [1 ]
Brodie, MJ [1 ]
机构
[1] Univ Glasgow, Western Infirm, Epilepsy Unit, Dept Med & Therapeut, Glasgow G11 6NT, Lanark, Scotland
关键词
antiepileptic drugs; mechanisms of action; epilepsy;
D O I
10.1016/S0163-7258(01)00122-X
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
In the past decade. nine new drugs have been licensed for the treatment of epilepsy. With limited clinical experience of these agents. the mechanisms of action of antiepileptic drugs may be an important criterion in the selection of the most suitable treatment regimens for individual patients, At the cellular level, three basic mechanisms are recognised: modulation of voltage-dependent ion channels, enhancement of inhibitory neurotransmission. and attenuation of excitatory transmission. In this review, we will attempt to introduce the concepts of ion channel and neurotransmitter modulation and, whereafter group currently used antiepileptic drugs according ro their principal mechanisms of action. (C) 2001 Elsevier Science Inc. All rights reserved.
引用
收藏
页码:21 / 34
页数:14
相关论文
共 174 条
[1]   Electrophysiologic analysis of the actions of valproate on pyramidal neurons in the rat hippocampal slice [J].
Albus, H ;
Williamson, R .
EPILEPSIA, 1998, 39 (02) :124-139
[2]  
[Anonymous], 1989, LANCET, V2, P196
[3]   Randomised, placebo-controlled study of vigabatrin as first-line treatment of infantile spasms [J].
Appleton, RE ;
Peters, ACB ;
Mumford, JP ;
Shaw, DE .
EPILEPSIA, 1999, 40 (11) :1627-1633
[4]   Ion channel mutations affecting muscle and brain [J].
Barchi, RL .
CURRENT OPINION IN NEUROLOGY, 1998, 11 (05) :461-468
[5]   Progress report on new antiepileptic drugs: a summary of the fourth Eilat conference (EILAT IV) [J].
Bialer, M ;
Johannessen, SI ;
Kupferberg, HJ ;
Levy, RH ;
Loiseau, P ;
Perucca, E .
EPILEPSY RESEARCH, 1999, 34 (01) :1-41
[6]   Levetiracetam (ucb L059) affects in vitro models of epilepsy in CA3 pyramidal neurons without altering normal synaptic transmission [J].
Birnstiel, S ;
Wulfert, E ;
Beck, SG .
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY, 1997, 356 (05) :611-618
[7]  
BORDEN LA, 1992, J BIOL CHEM, V267, P21098
[8]   TIAGABINE, SK-AND-F 89976-A, CI-966, AND NNC-711 ARE SELECTIVE FOR THE CLONED GABA TRANSPORTER GAT-1 [J].
BORDEN, LA ;
DHAR, TGM ;
SMITH, KE ;
WEINSHANK, RL ;
BRANCHEK, TA ;
GLUCHOWSKI, C .
EUROPEAN JOURNAL OF PHARMACOLOGY-MOLECULAR PHARMACOLOGY SECTION, 1994, 269 (02) :219-224
[9]   PRIMIDONE, PHENOBARBITAL, AND PEMA .1. SEIZURE PROTECTION, NEUROTOXICITY, AND THERAPEUTIC INDEX OF INDIVIDUAL COMPOUNDS IN MICE [J].
BOURGEOIS, BFD ;
DODSON, WE ;
FERRENDELLI, JA .
NEUROLOGY, 1983, 33 (03) :283-290
[10]   (R)-N-[4,4-BIS(3-METHYL-2-THIENYL)BUT-3-EN-1-YL]NIPECOTIC ACID BINDS WITH HIGH-AFFINITY TO THE BRAIN GAMMA-AMINOBUTYRIC ACID UPTAKE CARRIER [J].
BRAESTRUP, C ;
NIELSEN, EB ;
SONNEWALD, U ;
KNUTSEN, LJS ;
ANDERSEN, KE ;
JANSEN, JA ;
FREDERIKSEN, K ;
ANDERSEN, PH ;
MORTENSEN, A ;
SUZDAK, PD .
JOURNAL OF NEUROCHEMISTRY, 1990, 54 (02) :639-647