Shaikh Aasef G, Ramat Stefano, Optican Lance M, Miura Kenichiro, Leigh R John, Zee David S
Department of Neurology, The Johns Hopkins University, Baltimore, Maryland 21287, USA.
J Neuroophthalmol. 2008 Dec;28(4):329-36. doi: 10.1097/WNO.0b013e31818eb3a5.
Saccadic oscillations threaten clear vision by causing image motion on the retina. They are either purely horizontal (ocular flutter) or multidimensional (opsoclonus). We propose that ion channel dysfunction in the burst cell membrane is the underlying abnormality. We have tested this hypothesis by simulating a neuromimetic computational model of the burst neurons. This biologically realistic model mimics the physiologic properties and anatomic connections in the brainstem saccade generator. A rebound firing after sustained inhibition, called post-inhibitory rebound (PIR), and reciprocal inhibition between premotor saccadic burst neurons are the key features of this conceptual scheme. PIR and reciprocal inhibition make the circuits that generate the saccadic burst inherently unstable and can lead to oscillations unless stabilized by external inhibition. Our simulations suggest that alterations in membrane properties that lead to an increase in PIR, a reduction in external glycinergic inhibition, or both can cause saccadic oscillations.
扫视振荡通过在视网膜上引起图像运动而威胁清晰视力。它们要么是纯粹水平的（眼球扑动），要么是多维度的（眼阵挛）。我们提出，爆发细胞膜中的离子通道功能障碍是潜在的异常情况。我们通过模拟爆发神经元的神经模拟计算模型来检验这一假设。这个具有生物学现实意义的模型模仿了脑干扫视发生器中的生理特性和解剖连接。持续抑制后的反弹放电，称为抑制后反弹（PIR），以及运动前扫视爆发神经元之间的相互抑制是这一概念框架的关键特征。PIR和相互抑制使产生扫视爆发的电路本质上不稳定，并且除非通过外部抑制来稳定，否则会导致振荡。我们的模拟表明，导致PIR增加、外部甘氨酸能抑制减少或两者兼有的膜特性改变可引起扫视振荡。
