Relationship between thresholds to convulsions induced by a benzodiazepine inverse agonist and [3H]-L-glutamate binding in the membranes of brain regions

被引:2
作者
Conto, Marcos Brandao [1 ]
Barbosa de Carvalho, Jose Gilberto [1 ]
Campana Venditti, Marco Antonio [1 ]
机构
[1] Univ Fed Sao Paulo, Dept Psicobiol, Escola Paulista Med UNIFESP EPM, BR-04023062 Sao Paulo, Brazil
关键词
Convulsion; Seizure; H-3]-L-glutamate; Binding; Benzodiazepine inverse agonist; DMCM; GLUTAMATE; DIAZEPAM; RATS; GABA;
D O I
10.1007/s10072-012-1093-y
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Although some studies have investigated the influence of kindling model of epilepsy on the glutamatergic neurotransmission, the relation between glutamatergic receptors and seizure susceptibility remains unclear. The present study sought to determine if rats with high (HTR) and low (LTR) thresholds to clonic convulsions induced by the benzodiazepine inverse agonist DMCM differed in the [H-3]-l-glutamate binding to membranes from discrete brain regions. Compared to the HTR subgroup, the LTR subgroup presented a lower binding of [H-3]-l-glutamate in the hippocampus, frontal cortex and amygdala plus limbic cortex, suggesting that glutamatergic receptors in these brain regions may underlie the susceptibility to DMCM-induced convulsions.
引用
收藏
页码:537 / 538
页数:2
相关论文
共 10 条
[1]   Epilepsies in twins: Genetics of the major epilepsy syndromes [J].
Berkovic, SF ;
Howell, RA ;
Hay, DA ;
Hopper, JL .
ANNALS OF NEUROLOGY, 1998, 43 (04) :435-445
[2]   Glutamate, GABA and epilepsy [J].
Bradford, HF .
PROGRESS IN NEUROBIOLOGY, 1995, 47 (06) :477-511
[3]   Rats with different thresholds for DMCM-induced clonic convulsions differ in the sleep-time of diazepam and [3H]-Ro 15-4513 binding [J].
Conto, Marcos Brandao ;
Hipolide, Debora Cristina ;
Barbosa de Carvalho, Jose Gilberto ;
Campana Venditti, Marco Antonio .
EPILEPSY RESEARCH, 2012, 98 (2-3) :216-222
[4]   Diazepam binding inhibitor (DBI) in the plasma of pediatric and adult epileptic patients [J].
Ferrarese, C ;
Cogliati, T ;
Tortorella, R ;
Zucca, C ;
Bogliun, G ;
Beghi, E ;
Passoni, D ;
Zoia, C ;
Begni, B ;
Airoldi, L ;
Alho, H ;
Frattola, L .
EPILEPSY RESEARCH, 1998, 29 (02) :129-134
[5]   Seizures: Classification, etiologies, and pathophysiology [J].
March, PA .
CLINICAL TECHNIQUES IN SMALL ANIMAL PRACTICE, 1998, 13 (03) :119-131
[6]   MODULATION OF GABA-STIMULATED CL- FLUX BY A BENZODIAZEPINE AGONIST AND AN INVERSE AGONIST AFTER CHRONIC FLURAZEPAM TREATMENT [J].
NGUR, DO ;
ROSENBERG, HC ;
CHIU, TH .
EUROPEAN JOURNAL OF PHARMACOLOGY, 1990, 176 (03) :351-356
[7]   Benzodiazepine antagonists reduce epileptiform discharges in rat hippocampal slices [J].
Polc, P ;
Jahromi, SS ;
Facciponte, G ;
Pelletier, MR ;
Zhang, L ;
Carlen, PL .
EPILEPSIA, 1996, 37 (10) :1007-1014
[8]   Benzodiazepine receptor inverse agonist-induced kindling of rats alters learning and glutamate binding [J].
Rössler, AS ;
Schröder, H ;
Dodd, RH ;
Chapouthier, G ;
Grecksch, G .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 2000, 67 (01) :169-175
[9]   3H-L-glutamate binding and 3H-D-aspartate release from hippocampal tissue during the development of pentylenetetrazole kindling in rats [J].
Schröeder, H ;
Becker, A ;
Schröeder, U ;
Hoellt, V .
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR, 1999, 62 (02) :349-352
[10]   Neurochemistry and epileptology [J].
Van Rijn, Clementina ;
Meinardi, Harry .
EPILEPSIA, 2009, 50 :17-29