In vivo models of cortical acquired epilepsy

被引:27
|
作者
Chauvette, Sylvain [1 ]
Soltani, Sara [1 ,2 ]
Seigneur, Josee [1 ]
Timofeev, Igor [1 ,2 ]
机构
[1] CRIUSMQ, Local F-6500,2601 Canardiere, Quebec City, PQ G1J2G3, Canada
[2] Univ Laval, Dept Psychiat & Neurosci, Quebec City, PQ, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
Epilepsy; Epileptogenesis; Seizure; Trauma; Kindling; Undercut; TRAUMATIC BRAIN-INJURY; EXTRACELLULAR POTASSIUM ACTIVITY; SPIKE-WAVE COMPLEXES; PAROXYSMAL FAST RUNS; V PYRAMIDAL NEURONS; POSTTRAUMATIC EPILEPSY; NEOCORTICAL NEURONS; SEIZURE ACTIVITY; GAP-JUNCTIONS; ELECTRICAL-STIMULATION;
D O I
10.1016/j.jneumeth.2015.08.030
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
The neocortex is the site of origin of several forms of acquired epilepsy. Here we provide a brief review of experimental models that were recently developed to study neocortical epileptogenesis as well as some major results obtained with these methods. Most of neocortical seizures appear to be nocturnal and it is known that neuronal activities reveal high levels of synchrony during slow-wave sleep. Therefore, we start the review with a description of mechanisms of neuronal synchronization and major forms of synchronized normal and pathological activities. Then, we describe three experimental models of seizures and epileptogenesis: ketamine-xylazine anesthesia as feline seizure triggered factor, cortical undercut as cortical penetrating wound model and neocortical kindling. Besides specific technical details describing these models we also provide major features of pathological brain activities recorded during epileptogenesis and seizures. The most common feature of all models of neocortical epileptogenesis is the increased duration of network silent states that up-regulates neuronal excitability and eventually leads to epilepsy. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:185 / 201
页数:17
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