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视网膜中多巴胺释放的调控:神经网络的转基因方法

Control of dopamine release in the retina: a transgenic approach to neural networks.

作者信息

Gustincich S, Feigenspan A, Wu D K, Koopman L J, Raviola E

机构信息

Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA.

出版信息

Neuron. 1997 May;18(5):723-36. doi: 10.1016/s0896-6273(00)80313-x.

DOI:10.1016/s0896-6273(00)80313-x
PMID:9182798
Abstract

Dopaminergic, interplexiform amacrines (DA cells) were labeled in transgenic mice with human placental alkaline phosphatase, an enzyme that resides on the outer surface of the cell membrane. It was therefore possible to investigate their activity in vitro after dissociation of the retina with whole-cell current and voltage clamp, as well as their connections in the intact retina with the electron microscope. DA cells generate action potentials even in the absence of synaptic inputs. This activity is abolished by the amacrine cell transmitters GABA and glycine, which induce an inward current carried by chloride ions, and is stimulated by kainate, an agonist at the receptor for the bipolar cell transmitter glutamate, which opens nonselective cation channels. Since DA cells are postsynaptic to amacrine and bipolar cells, we suggest that the spontaneous discharge of DA cells is inhibited in the dark by GABAergic amacrines that receive their input from off-bipolars. Upon illumination, the GABA-inhibition is removed, DA cells generate action potentials, and their firing is modulated by the excitation received from on-bipolars.

摘要

在转基因小鼠中,用人类胎盘碱性磷酸酶标记多巴胺能、网间无长突细胞(DA细胞),该酶位于细胞膜外表面。因此,在视网膜解离后,利用全细胞电流和电压钳可以在体外研究它们的活性,同时利用电子显微镜可以研究它们在完整视网膜中的连接。即使在没有突触输入的情况下,DA细胞也能产生动作电位。无长突细胞递质γ-氨基丁酸(GABA)和甘氨酸可消除这种活性,它们诱导氯离子携带的内向电流,而双极细胞递质谷氨酸受体的激动剂 kainate 可刺激这种活性,kainate 可打开非选择性阳离子通道。由于DA细胞是无长突细胞和双极细胞的突触后细胞,我们认为在黑暗中,DA细胞的自发放电受到来自离双极细胞接收输入的GABA能无长突细胞的抑制。光照时,GABA抑制作用被消除,DA细胞产生动作电位,其放电受到来自开双极细胞的兴奋调节。

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