The neurobiology of antiepileptic drugs

被引：894
作者：
Rogawski, MA [1 ]
Löscher, W
机构：
[1] NINDS, Epilepsy Res Stn, NIH, Bethesda, MD 20892 USA
[2] Univ Vet Med, Dept Pharmacol Toxicol & Pharm, D-30559 Hannover, Germany
[3] Ctr Syst Neurosci, D-30559 Hannover, Germany
来源：
NATURE REVIEWS NEUROSCIENCE | 2004年 / 5卷 / 07期
关键词：
D O I：
10.1038/nrn1430
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Antiepileptic drugs (AEDs) provide satisfactory control of seizures for most patients with epilepsy. The drugs have the remarkable ability to protect against seizures while permitting normal functioning of the nervous system. AEDs act on diverse molecular targets to selectively modify the excitability of neurons so that seizure-related firing is blocked without disturbing non-epileptic activity. This occurs largely through effects on voltage-gated sodium and calcium channels, or by promoting inhibition mediated by GABA(A) (gamma-aminobutyric acid, type A) receptors. The subtle biophysical modifications in channel behaviour that are induced by AEDs are often functionally opposite to defects in channel properties that are caused by mutations associated with epilepsy in humans.
引用
收藏
页码：553 / 564
页数：12
相关论文
共 144 条
[1]   Increased persistent sodium currents in rat entorhinal cortex layer V neurons in a post-status epilepticus model of temporal lobe epilepsy [J].
Agrawal, N ;
Alonso, A ;
Ragsdale, DS .
EPILEPSIA, 2003, 44 (12) :1601-1604
[2]   DIFFERENTIAL-EFFECTS OF EXTRACELLULAR AND INTRACELLULAR ANIONS ON GABA-ACTIVATED CURRENTS IN BULLFROG SENSORY NEURONS [J].
AKAIKE, N ;
INOMATA, N ;
YAKUSHIJI, T .
JOURNAL OF NEUROPHYSIOLOGY, 1989, 62 (06) :1388-1399
[3]   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
[4]   Enhanced inactivation and acceleration of activation of the sodium channel associated with epilepsy in man [J].
Alekov, AK ;
Rahman, M ;
Mitrovic, N ;
Lehmann-Horn, F ;
Lerche, H .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2001, 13 (11) :2171-2176
[5]   Inhibition of glutamate release by BIA 2-093 and BIA 2-024, two novel derivatives of carbamazepine, due to blockade of sodium but not calcium channels [J].
Ambósio, AF ;
Silva, AP ;
Malva, JO ;
Soares-da-Silva, P ;
Carvalho, AP ;
Carvalho, CM .
BIOCHEMICAL PHARMACOLOGY, 2001, 61 (10) :1271-1275
[6]   Auxiliary subunits: essential components of the voltage-gated calcium channel complex [J].
Arikkath, J ;
Campbell, KP .
CURRENT OPINION IN NEUROBIOLOGY, 2003, 13 (03) :298-307
[7]   Distinct functional and pharmacological properties of tonic and quantal inhibitory postsynaptic currents mediated by γ-aminobutyric acidA receptors in hippocampal neurons [J].
Bai, DL ;
Zhu, GY ;
Pennefather, P ;
Jackson, MF ;
Macdonald, JF ;
Orser, BA .
MOLECULAR PHARMACOLOGY, 2001, 59 (04) :814-824
[8]   First genetic evidence of GABAA receptor dysfunction in epilepsy:: a mutation in the γ2-subunit gene [J].
Baulac, S ;
Huberfeld, G ;
Gourfinkel-An, I ;
Mitropoulou, G ;
Beranger, A ;
Prud'homme, JF ;
Baulac, M ;
Brice, A ;
Bruzzone, R ;
LeGuern, E .
NATURE GENETICS, 2001, 28 (01) :46-48
[9]  
BAZIL CW, 2002, ANTIEPILEPTIC DRUGS, P22
[10]  
Bianchi MT, 2002, J NEUROSCI, V22, P5321
12345678910