2018年8月1日
Control of excessive neural circuit excitability and prevention of epileptic seizures by endocannabinoid signaling
Cellular and Molecular Life Sciences
- ,
- 巻
- 75
- 号
- 15
- 開始ページ
- 2793
- 終了ページ
- 2811
- 記述言語
- 英語
- 掲載種別
- DOI
- 10.1007/s00018-018-2834-8
- 出版者・発行元
- Birkhauser Verlag AG
Progress in research on endocannabinoid signaling has greatly advanced our understanding of how it controls neural circuit excitability in health and disease. In general, endocannabinoid signaling at excitatory synapses suppresses seizures by inhibiting glutamate release. In contrast, endocannabinoid signaling promotes seizures by inhibiting GABA release at inhibitory synapses. The physiological distribution of endocannabinoid signaling molecules becomes disrupted with the development of epileptic focus in patients with mesial temporal lobe epilepsy and in animal models of experimentally induced epilepsy. Augmentation of endocannabinoid signaling can promote the development of epileptic focus at initial stages. However, at later stages, increased endocannabinoid signaling delays it and suppresses spontaneous seizures. Thus, the regulation of endocannabinoid signaling at specific synapses that cause hyperexcitability during particular stages of disease development may be effective for treating epilepsy and epileptogenesis.
- リンク情報
- ID情報
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- DOI : 10.1007/s00018-018-2834-8
- ISSN : 1420-9071
- ISSN : 1420-682X
- PubMed ID : 29737364
- SCOPUS ID : 85046661127