Differential paired-pulse responses between the CA1 region and the dentate gyrus are related to altered CLC-2 immunoreactivity in the pilocarpine-induced rat epilepsy model

被引:19
作者
Kwak, Sung-Eun
Kim, Ji-Eun
Kim, Duk-Soo
Won, Moo Ho
Lee, Hong Jin
Choi, Soo-Young
Kwon, Oh-Shin
Kim, Jin-Sang
Kang, Tae-Cheon [1 ]
机构
[1] Hallym Univ, Dept Anat, Coll Med, Chunchon 200702, Kangwon Do, South Korea
[2] Hallym Univ, Dept Pediat, Coll Med, Chunchon 200702, Kangwon Do, South Korea
[3] Hallym Univ, Dept Genet Engn, Coll Life Sci, Chunchon 200702, Kangwon Do, South Korea
[4] Kyungpook Natl Univ, Dept Biochem, Coll Nat Sci, Taegu 702701, South Korea
[5] Daegu Univ, Dept Phys Therapy, Coll Rehabil Sci, Taegu 705714, South Korea
关键词
CLC-2; dentate gyrus; hippocampus; epilepsy; paired-pulse inhibition;
D O I
10.1016/j.brainres.2006.07.082
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The epileptic hippocampus shows differential paired-pulse responses between the dentate gyrus and the CA1 region. However, little data are available to explain this phenomenon. In the present study, we identified the relationship between regional differences of paired-pulse response and voltage gated Cl- channel 2 (CLC-2)/vesicular GABA transport (VGAT) expression in a pilocarpine-induced rat model. During epileptogenic periods, paired-pulse inhibitions in the dentate gyrus and the CA1 region were markedly reduced. After recurrent seizure onset, paired-pulse inhibition in the dentate gyrus was markedly enhanced, while that in the CA1 region more reduced. Unlike VGAT, CLC-2 immunoreactivity was markedly reduced in the hippocampus during epileptogenic periods and was re-enhanced only in the dentate gyrus after recurrent seizure onset. Linear regression analysis showed an inverse proportional relationship between alterations in CLC-2 immunoreactivity and changes in normalized population spike amplitude ratio within the CA1 region and the dentate gyrus. Therefore, our findings suggest that the regionally specific alterations in CLC-2 immunoreactivity after SE may determine the properties of paired-pulse responses in the hippocampus of the pilocarpine-induced rat epilepsy model. (c) 2006 Elsevier B.V. All rights reserved.
引用
收藏
页码:162 / 168
页数:7
相关论文
共 33 条
[1]   Vigabatrin protects against hippocampal damage but is not antiepileptogenic in the lithium-pilocarpine model of temporal lobe epilepsy [J].
André, V ;
Ferrandon, A ;
Marescaux, C ;
Nehlig, A .
EPILEPSY RESEARCH, 2001, 47 (1-2) :99-117
[2]   DORMANCY OF INHIBITORY INTERNEURONS IN A MODEL OF TEMPORAL-LOBE EPILEPSY [J].
BEKENSTEIN, JW ;
LOTHMAN, EW .
SCIENCE, 1993, 259 (5091) :97-100
[3]   Selective changes in single cell GABAA receptor subunit expression and function in temporal lobe epilepsy [J].
Brooks-Kayal, AR ;
Shumate, MD ;
Jin, H ;
Rikhter, TY ;
Coulter, DA .
NATURE MEDICINE, 1998, 4 (10) :1166-1172
[4]   Zinc-induced collapse of augmented inhibition by GABA in a temporal lobe epilepsy model [J].
Buhl, EH ;
Otis, TS ;
Mody, I .
SCIENCE, 1996, 271 (5247) :369-373
[5]   Developmental expression of ClC-2 in the rat nervous system [J].
Clayton, GH ;
Staley, KJ ;
Wilcox, CL ;
Owens, GC ;
Smith, RL .
DEVELOPMENTAL BRAIN RESEARCH, 1998, 108 (1-2) :307-318
[6]   Dentate granule cell GABAA receptors in epileptic hippocampus:: enhanced synaptic efficacy and altered pharmacology [J].
Cohen, AS ;
Lin, DD ;
Quirk, GL ;
Coulter, DA .
EUROPEAN JOURNAL OF NEUROSCIENCE, 2003, 17 (08) :1607-1616
[7]   Increased expression of the Drosophila vesicular glutamate transporter leads to excess glutamate release and a compensatory decrease in quantal content [J].
Daniels, RW ;
Collins, CA ;
Gelfand, MV ;
Dant, J ;
Brooks, ES ;
Krantz, DE ;
DiAntonio, A .
JOURNAL OF NEUROSCIENCE, 2004, 24 (46) :10466-10474
[8]   HIPPOCAMPAL INTERNEURON LOSS AND PLASTICITY IN HUMAN TEMPORAL-LOBE EPILEPSY [J].
DELANEROLLE, NC ;
KIM, JH ;
ROBBINS, RJ ;
SPENCER, DD .
BRAIN RESEARCH, 1989, 495 (02) :387-395
[9]   Reduced excitatory drive onto interneurons in the dentate gyrus after status epilepticus [J].
Doherty, J ;
Dingledine, R .
JOURNAL OF NEUROSCIENCE, 2001, 21 (06) :2048-2057
[10]  
Gulácsi A, 2003, J NEUROSCI, V23, P8237