Experimental Models of Absence Epilepsy

被引:10
作者
Jafarian, Maryam [1 ,2 ]
Alipour, Mohammad Esmaeil [3 ]
Karimzadeh, Fariba [4 ]
机构
[1] Univ Tehran Med Sci, Brain & Spinal Cord Injury Res Ctr, Neurosci Inst, Tehran, Iran
[2] Khatam Alanbia Hosp, Shefa Neurosci Res Ctr, Tehran, Iran
[3] Univ Tehran Med Sci, Sch Adv Technol Med, Dept Neurosci & Addict Studies, Tehran, Iran
[4] Iran Univ Med Sci, Cellular & Mol Res Ctr, Tehran, Iran
关键词
Epilepsy; Absence; Animal models; Seizures; Genetic models; SPIKE-WAVE DISCHARGES; GENETIC RAT MODEL; ANIMAL-MODELS; THALAMIC NEURONS; MUTANT MOUSE; SEIZURES; EXPRESSION; MUTATIONS; SUBUNIT; PHARMACOLOGY;
D O I
10.32598/bcn.11.6.731.1
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Introduction: Absence epilepsy is a brief non-convulsive seizure associated with sudden abruptness in consciousness. Because of the unpredictable occurrence of absence seizures and the ethical issues of human investigation on the pathogenesis and drug assessment, researchers tend to study animal models. This paper aims to review the advantages and disadvantages of several animal models of nonconvulsive induced seizure. Methods: The articles that were published since 1990 were assessed. The publications that used genetic animals were analyzed, too. Besides, we reviewed possible application methods of each model, clinical types of seizures induced, purposed mechanism of epileptogenesis, their validity, and relevance to the absence epileptic patients. Results: The number of studies that used genetic models of absence epilepsy from years of 2000 was noticeably more than pharmacological models. Genetic animal models have a close correlation of electroencephalogram features and epileptic behaviors to the human condition. Conclusion: The validity of genetic models of absence epilepsy would motivate the researchers to focus on genetic modes in their studies. As there are some differences in the pathophysiology of absence epilepsy between animal models and humans, the development of new animal models is necessary to understand better the epileptogenic process and, or discover novel therapies for this disorder.
引用
收藏
页码:715 / 726
页数:12
相关论文
共 69 条
[1]   CALCIUM-DEPENDENT REGULATION OF GENETICALLY-DETERMINED SPIKE AND WAVES BY THE RETICULAR THALAMIC NUCLEUS OF RATS [J].
AVANZINI, G ;
VERGNES, M ;
SPREAFICO, R ;
MARESCAUX, C .
EPILEPSIA, 1993, 34 (01) :1-7
[2]   AN ANALYSIS OF PENICILLIN-INDUCED GENERALIZED SPIKE AND WAVE DISCHARGES USING SIMULTANEOUS RECORDINGS OF CORTICAL AND THALAMIC SINGLE NEURONS [J].
AVOLI, M ;
GLOOR, P ;
KOSTOPOULOS, G ;
GOTMAN, J .
JOURNAL OF NEUROPHYSIOLOGY, 1983, 50 (04) :819-837
[3]   Ducky mouse phenotype of epilepsy and ataxia is associated with mutations in the Cacna2d2 gene and decreased calcium channel current in cerebellar Purkinje cells [J].
Barclay, J ;
Balaguero, N ;
Mione, M ;
Ackerman, SL ;
Letts, VA ;
Brodbeck, J ;
Canti, C ;
Meir, A ;
Page, KM ;
Kusumi, K ;
Perez-Reyes, E ;
Lander, ES ;
Frankel, WN ;
Gardiner, RM ;
Dolphin, AC ;
Rees, M .
JOURNAL OF NEUROSCIENCE, 2001, 21 (16) :6095-6104
[4]   ANTAGONISM OF GAMMA-HYDROXYBUTYRIC ACID-INDUCED FREQUENCY-SHIFTS IN THE CORTICAL EEG OF RATS BY DIPROPYLACETATE [J].
BEARDEN, LJ ;
SNEAD, OC ;
HEALEY, CT ;
PEGRAM, GV .
ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY, 1980, 49 (1-2) :181-183
[5]   Revised terminology and concepts for organization of seizures and epilepsies: Report of the ILAE Commission on Classification and Terminology, 2005-2009 [J].
Berg, Anne T. ;
Berkovic, Samuel F. ;
Brodie, Martin J. ;
Buchhalter, Jeffrey ;
Cross, J. Helen ;
Boas, Walter van Emde ;
Engel, Jerome ;
French, Jacqueline ;
Glauser, Tracy A. ;
Mathern, Gary W. ;
Moshe, Solomon L. ;
Nordli, Douglas ;
Plouin, Perrine ;
Scheffer, Ingrid E. .
EPILEPSIA, 2010, 51 (04) :676-685
[6]  
Berkovic SF., 1994, Epilepsies in twins. Epileptic seizures and syndromes, P157
[7]   Cellular and network mechanisms of spike-wave seizures [J].
Blumenfeld, H .
EPILEPSIA, 2005, 46 :21-33
[8]   Splicing of α1A subunit gene generates phenotypic variants of P- and Q-type calcium channels [J].
Bourinet, E ;
Soong, TW ;
Sutton, K ;
Slaymaker, S ;
Mathews, E ;
Monteil, A ;
Zamponi, GW ;
Nargeot, J ;
Snutch, TP .
NATURE NEUROSCIENCE, 1999, 2 (05) :407-415
[9]  
Budde T, 2006, MODELS OF SEIZURES AND EPILEPSY, P73, DOI 10.1016/B978-012088554-1/50009-8
[10]   Single gene defects in mice: the role of voltage-dependent calcium channels in absence models [J].
Burgess, DL ;
Noebels, JL .
EPILEPSY RESEARCH, 1999, 36 (2-3) :111-122