Center for Glial-Neuronal Interactions, Division of Biomedical Sciences, University of California, Riverside, California 92521-0121, USA.
Glia. 2012 Aug;60(8):1203-14. doi: 10.1002/glia.22317. Epub 2012 Feb 29.
Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4(-/-) mice) or α-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets.
最近的研究表明神经胶质细胞在突触传递的调节中起作用,因此神经胶质细胞在癫痫的过度兴奋特征中可能具有功能作用是合理的。事实上,星形胶质细胞膜通道、受体和转运体的改变都与癫痫状态有关。这篇综述重点介绍了水通道蛋白 4 (AQP4) 在调节大脑兴奋性和癫痫中的潜在作用。我们将回顾缺乏 AQP4 (Aqp4(-/-) 小鼠)或α-突触核蛋白 (AQP4 的锚定蛋白)的小鼠的研究,并讨论现有的人类研究表明 AQP4 在人类癫痫组织标本中的改变。我们将以 AQP4 调节的新研究结束,并讨论 AQP4 在癫痫发生(癫痫发生)中的潜在作用。虽然仍有许多问题尚未得到解答,但现有数据表明 AQP4 及其分子伴侣可能代表着重要的新治疗靶点。