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光可诱发视网膜双极细胞轴突终末产生钙离子峰电位。

Light evokes Ca2+ spikes in the axon terminal of a retinal bipolar cell.

作者信息

Protti D A, Flores-Herr N, von Gersdorff H

机构信息

Max-Planck Institute for Biophysical Chemistry, Göttingen, Germany.

出版信息

Neuron. 2000 Jan;25(1):215-27. doi: 10.1016/s0896-6273(00)80884-3.

DOI:10.1016/s0896-6273(00)80884-3
PMID:10707985
Abstract

Bipolar cells in the vertebrate retina have been characterized as nonspiking interneurons. Using patch-clamp recordings from goldfish retinal slices, we find, however, that the morphologically well-defined Mb1 bipolar cell is capable of generating spikes. Surprisingly, in dark-adapted retina, spikes were reliably evoked by light flashes and had a long (1-2 s) refractory period. In light-adapted retina, most Mb1 cells did not spike. However, an L-type Ca2+ channel agonist could induce periodic spiking in these cells. Spikes were determined to be Ca2+ action potentials triggered at the axon terminal and were abolished by 2-amino-4-phosphonobutyric acid (APB), an agonist that mimics glutamate. Signaling via spikes in a specific class of bipolar cells may serve to accelerate and amplify small photo-receptor signals, thereby securing the synaptic transmission of dim and rapidly changing visual input.

摘要

脊椎动物视网膜中的双极细胞被描述为无动作电位的中间神经元。然而,通过对金鱼视网膜切片进行膜片钳记录,我们发现形态明确的Mb1双极细胞能够产生动作电位。令人惊讶的是,在暗适应的视网膜中,光刺激能可靠地诱发动作电位,且具有较长(1 - 2秒)的不应期。在光适应的视网膜中,大多数Mb1细胞不产生动作电位。然而,一种L型Ca2+通道激动剂可诱导这些细胞产生周期性动作电位。动作电位被确定为由轴突末端触发的Ca2+动作电位,并被模拟谷氨酸的激动剂2 - 氨基 - 4 - 膦酰丁酸(APB)所消除。特定类型双极细胞通过动作电位进行信号传递,可能有助于加速和放大微小的光感受器信号,从而确保昏暗且快速变化的视觉输入的突触传递。

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