流行病学数据和基因关联研究表明,遗传易感性是后天脑损伤(如脑外伤)后发展为癫痫的主要病因。因此,对遗传易感性进行深入的了解将会对疾病的早期诊断和预后,以及开发靶向抗癫痫药物(AEDs)和优化临床试验设计具有巨大的帮助。在实验室中,调查部分人群更易发展为获得性癫痫的方法是建立表现出易感性或对癫痫发生具有抵抗力的独特啮齿动物模型。本综述着重于这些模型中最具代表性的模型,即 FAST(快点燃)和 SLOW(慢点燃)大鼠品系,它们是通过选择性育种具有不同的杏仁核电点燃率筛选出来的。文章描述了这些品系在基线和脑损伤后的癫痫发作特征、神经解剖学和神经行为表型的不同之处,被证明可用于识别与癫痫发作易感性和精神类疾病合并症相关的常见的病理异常。值得注意的是,尽管在多个生物学过程中获得的品系数据差异可说明部分人群更易发生癫痫的原因,但仍需进一步研究以确定确切的分子和遗传危险因素。FAST 和 SLOW 大鼠品系以及其他类似的实验模型,是研究遗传背景对发展为获得性癫痫风险以及癫痫发展与相关合并症之间关系的宝贵的神经生物学工具。
Citation: LeungWL, Casillas-EspinosaP, SharmaP, 张颖颖, 慕洁. 获得性癫痫的遗传易感性的动物模型:快点燃和慢点燃大鼠. Journal of Epilepsy, 2020, 6(4): 354-365. doi: 10.7507/2096-0247.20200058 Copy
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- 1. Engel J Jr. Introduction to temporal lobe epilepsy. Epilepsy Res, 1996, 26(1): 141-150.
- 2. Thomas RH, Berkovic SF. The hidden genetics of epilepsy‐a clinically important new paradigm. Nat Rev Neurol, 2014, 10(5): 283-292.
- 3. Pitkänen A, Sutula T. Is epilepsy a progressive disorder? Prospects for new therapeutic approaches in temporal‐lobe epilepsy. Lancet Neurol, 2002, 1(3): 173-181.
- 4. Powell K, Lukasiuk K, O'Brien T, et al. Are alterations in transmitter receptor and ion channel expression responsible for epilepsies? Adv Exp Med Biol, 2014, 2014, 813: 211-229.
- 5. Herman ST. Epilepsy after brain insult: targeting epileptogenesis. Neurology, 2002, 59(Suppl 5): 21-26.
- 6. Lowenstein DH. Recent advances related to basic mechanisms of epileptogenesis. Epilepsy Res, 1996, 11(Suppl): 45-60.
- 7. Löscher W. Animal models of seizures and epilepsy: past, present, and future role for the discovery of antiseizure drugs. Neurochem Res, 2017, 42(7): 1873-1888.
- 8. Brooks Kayal A, Raol Y, Russek S. Alteration of epileptogenesis genes. Neurotherapeutics, 2009, 6(2): 312-318.
- 9. Christensen J, Pedersen MG, Pedersen CB, et al. Long‐term risk of epilepsy after traumatic brain injury in children and young adults: a population‐based cohort study. Lancet, 2009, 373(9669): 1105-1110.
- 10. Kobow K, Auvin S, Jensen F, et al. Finding a better drug for epilepsy: antiepileptogenesis targets. Epilepsia, 2012, 53(11): 1868-1876.
- 11. McNamara JO, Huang YZ, Leonard AS. Molecular signaling mechanisms underlying epileptogenesis. Sci STKE, 2006: re12.
- 12. Ritter A, Kammerer C, Brooks M, et al. Genetic variation in neuronal glutamate transport genes and associations with posttraumatic seizure. Epilepsia, 2016, 57(6): 984-993.
- 13. Arion D, Sabatini M, Unger T, et al. Correlation of transcriptome profile with electrical activity in temporal lobe epilepsy. Neurobiol Dis, 2006, 22(2): 374-387.
- 14. Berkovic S, Mulley J, Scheffer I, et al. Human epilepsies: interaction of genetic and acquired factors. Trends Neurosci, 2006, 29(7): 391-397.
- 15. Diamond M, Ritter A, Jackson E, et al. Genetic variation in the adenosine regulatory cycle is associated with posttraumatic epilepsy development. Epilepsia, 2015, 56(8): 1198-1206.
- 16. Cotter D, Kelso A, Neligan A. Genetic biomarkers of posttraumatic epilepsy: a systematic review. Seizure, 2017, 46: 53-58.
- 17. Racine RJ, Steingart M, McIntyre DC. Development of kindlingprone and kindling‐resistant rats: selective breeding and electrophysiological studies. Epilepsy Res, 1999, 35(3): 183-195.
- 18. Rimoin DL, Metrakos JD. The genetics of convulsive disorders in the families of hemiplegics. Proc 2nd Intern Congr Hum Genet. Rome: Institute G. Mendel, 1963: 1655-1658.
- 19. Darrah SD, Miller MA, Ren D, et al. Genetic variability in glutamic acid decarboxylase genes: associations with post‐traumatic seizures after severe TBI. Epilepsy Res, 2013, 103(2-3): 180-194.
- 20. Scher AI, Wu H, Tsao JW, et al. MTHFR C677T genotype as a risk factor for epilepsy including post‐traumatic epilepsy in a representative military cohort. J Neurotrauma, 2011, 28(9): 1739-1745.
- 21. Wagner AK, Miller MA, Scanlon J, et al. Adenosine A1 receptor gene variants associated with post‐traumatic seizures after severe TBI. Epilepsy Res, 2010, 90(3): 259-272.
- 22. Kuo PH, Kalsi G, Prescott CA, et al. Associations of glutamate decarboxylase genes with initial sensitivity and age‐at‐onset of alcohol dependence in the Irish Affected Sib Pair Study of Alcohol Dependence. Drug Alcohol Depend, 2009, 101(1-2): 80-87.
- 23. Franklin PH, Zhang G, Tripp ED, et al. Adenosine A1 receptor activation mediates suppression of (‐) bicuculline methiodide‐induced seizures in rat prepiriform cortex. J Pharmacol Exp Ther, 1989, 251: 1229-1236.
- 24. Alyu F, Dikmen M. Inflammatory aspects of epileptogenesis: contribution of molecular inflammatory mechanisms. Acta Neuropsychiatr, 2017, 29(1): 1-16.
- 25. Saletti P, Ali I, Casillas Espinosa P, et al. In search of antiepileptogenic treatments for post‐traumatic epilepsy. Neurobiol Dis, 2018, 123: 86-99.
- 26. Fu CY, Chen SJ, Cai NH, et al. Increased risk of post‐stroke epilepsy in Chinese patients with a TRPM6 polymorphism. Neurol Res, 2019, 41(4): 378-383.
- 27. Yang H, Song Z, Yang GP, et al. The ALDH2 rs671 polymorphism affects post‐stroke epilepsy susceptibility and plasma 4‐HNE levels. PLoS ONE, 2014, 9: e109634.
- 28. Szyndler J, Maciejak P, Turzynska D, et al. The effects of electrical hippocampal kindling of seizures on amino acids and kynurenic acid concentrations in brain structures. J Neural Transm (Vienna), 2012, 119: 141-149.
- 29. Morimoto K, Fahnestock M, Racine RJ. Kindling and status epilepticus models of epilepsy: rewiring the brain. Prog Neurobiol, 2004, 73(1): 1-60.
- 30. Racine RJ. Modification of seizure activity by electrical stimulation. II. Motor Seizure. Electroencephalogr Clin Neurophysiol, 1972, 32(3): 281-294.
- 31. McIntyre DC, Kent P, Hayley S, et al. Influence of psychogenic and neurogenic stressors on neuroendocrine and central monoamine activity in fast and slow kindling rats. Brain Res, 1999, 840(1-2): 65-74.
- 32. Racine RJ, Burnham WM, Gartner JG, et al. Rates of motor seizure development in rats subjected to electrical brain stimulation: strain and inter‐stimulation interval effects. Electroencephalogr Clin Neurophysiol, 1973, 35(5): 553-556.
- 33. McIntyre DC, Kelly ME, Dufresne C. FAST and SLOW amygdala kindling rat strains: comparison of amygdala, hippocampal, piriform and perirhinal cortex kindling. Epilepsy Res, 1999, 35(3): 197-209.
- 34. Baker BL, Neece CL, Fenning RM, et al. Mental disorders in five‐year‐old children with or without developmental delay: focus on ADHD. J Clin Child Adolesc Psychol, 2010, 39(4): 492-505.
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