Epilepsy research. Supplement最新文献_第2页

Abnormal frequency-selective domains in inferior colliculus of audiogenic seizure susceptible rats. 听原性癫痫易感大鼠下丘频率选择域异常。

Epilepsy research. Supplement Pub Date : 1996-01-01

M Pierson, A Snyder-Keller, J Kwon

引用次数: 0

Basic mechanisms of seizure propagation: targets for rational drug design and rational polypharmacy. 癫痫传播的基本机制:合理药物设计和合理多药的靶点。

Epilepsy research. Supplement Pub Date : 1996-01-01

W Löscher, U Ebert

引用次数: 0

Use of animal models in developing guiding principles for polypharmacy in epilepsy. 动物模型在制定癫痫多药治疗指导原则中的应用。

Epilepsy research. Supplement Pub Date : 1996-01-01

W Löscher, A Wauquier

引用次数: 0

GABAA inhibition controls the calcium flows during NMDA-dependent epileptiform activity in human epileptogenic neocortex. GABAA抑制控制nmda依赖性癫痫样活动在人致痫性新皮层中的钙流动。

Epilepsy research. Supplement Pub Date : 1996-01-01

J Louvel, R Pumain, M Avoli, I Kurcewicz, B Devaux, J P Chodkiewicz

引用次数: 0

Hyperexcitability after focal lesions and transient ischemia in rat neocortex. 大鼠大脑皮层局灶性损伤后的高兴奋性和短暂性缺血。

Epilepsy research. Supplement Pub Date : 1996-01-01

H J Luhmann, T Mittmann, R Schmidt-Kastner, U T Eysel, L A Mudrick-Donnon, U Heinemann

引用次数: 0

Excitability changes in thalamic and neocortical neurons after injury. 损伤后丘脑和新皮质神经元兴奋性的变化。

Epilepsy research. Supplement Pub Date : 1996-01-01

J R Huguenard, J M Chung, D A Prince

引用次数: 0

Status epilepticus and the late development of spontaneous seizures in the pilocarpine model of epilepsy. 匹罗卡平癫痫模型中癫痫持续状态和自发性发作的晚期发展。

Epilepsy research. Supplement Pub Date : 1996-01-01

T Lemos, E A Cavalheiro

引用次数: 0

Recent advances related to basic mechanisms of epileptogenesis. 癫痫发生的基本机制研究进展。

Epilepsy research. Supplement Pub Date : 1996-01-01

D H Lowenstein

{"title":"Recent advances related to basic mechanisms of epileptogenesis.","authors":"D H Lowenstein","doi":"","DOIUrl":"","url":null,"abstract":"A variety of clinical observations suggest that certain forms of epilepsy are due to long-term, progressive changes in neural networks that eventually provoke spontaneous and recurring seizures. This process of network transformation, known as epileptogenesis, is a potentially important therapeutic target and also serves as an extremely interesting model of central nervous system plasticity. This article reviews some of the significant, recent advances in our understanding of mechanisms underlying epileptogenesis in different forms of epilepsy. The most substantial progress has been made in work related to temporal lobe epilepsy (TLE), where the biochemical, electrophysiological and anatomical changes in the hippocampus have been intensively studied. This has led to a number of cogent and testable hypotheses, including the concept that dentate granule cell hyperexcitability in TLE is due to a selective loss of hilar neurons that renders inhibitory cells 'dormant.' Studies of other forms of focal epilepsy suggest that a seizure focus may develop as a result of axonal reorganization or immune-mediated effects on membrane channels. Epileptogenesis in generalized epilepsies remains poorly understood, although recent work using models of absence epilepsy point to the critical role of GABAB or T-type calcium channels in the thalamus. Also, new transgenic mouse lines with epilepsy phenotypes have introduced candidate genes, such as those encoding the serotonin 5-HT2C receptor or the alpha subunit of calcium/calmodulin kinase II, that may be responsible for epileptogenesis. Finally, a large amount of investigation has focused on seizure-induced gene expression and it is now clear that seizures can cause a cascade of changes in the expression of gene products that are likely to play a role in network plasticity. Progress in developing 'anti-epileptogenic' therapies will require further advances in understanding the mechanistic roles of these various biochemical and anatomical changes in the transformation of normal to hyperexcitable neural networks.","PeriodicalId":77115,"journal":{"name":"Epilepsy research. Supplement","volume":"11 ","pages":"45-60"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20236358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correlation of epilepsy syndromes and basic mechanisms. 癫痫综合征的相关性及基本机制。

Epilepsy research. Supplement Pub Date : 1996-01-01

P Wolf

{"title":"Correlation of epilepsy syndromes and basic mechanisms.","authors":"P Wolf","doi":"","DOIUrl":"","url":null,"abstract":"To combine both clinical and experimental findings into comprehensive nosological theories is a novel approach in epileptology, the adoption of which seems highly advisable for future research. A selection of problems concerning some well-known epilepsy syndromes are presented which could profit from such an approach. In idiopathic epilepsies, both generalized and localization-related, there seems to be an astonishing amount of variability beyond the acknowledged syndromes when these are looked at in detail. Much of this variance seems to be the consequence of regional expression of the genes which are certainly involved in their pathogenesis. Some of the involved genes seem to have not only a spatial but also a temporal limit of action. In symptomatic and cryptogenic 'generalized' epilepsies the rôle of focal etiological factors needs to be clarified as well as the question why their phenotype seems to depend more upon the manifestation age than the etiology. In relation to the symptomatic and cryptogenic focal epilepsies, it becomes more and more intriguing whether they are all due to more or less identical interactions of a set of basic mechanisms or whether foci in different cortical areas differ in this respect. It appears that there are many syndrome-related or syndrome-specific differences in the rôle of basic mechanisms in human epilepsies. A better understanding of these differences could become most helpful for the development of more specific and more effective therapies.","PeriodicalId":77115,"journal":{"name":"Epilepsy research. Supplement","volume":"11 ","pages":"141-51"},"PeriodicalIF":0.0,"publicationDate":"1996-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20236365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fos-like immunoreactivity after status epilepticus and spontaneous seizures in rats. 大鼠癫痫持续状态和自发性发作后fos样免疫反应性。

Epilepsy research. Supplement Pub Date : 1996-01-01

L E Mello, A M Tan, D M Finch, C M Kohman, E A Cavalheiro

引用次数: 0