tetrodotoxin-resistant sodium channels contribute to directional responses in starburst amacrine cellstetrodotoxin-resistant钠离子通道为定向反应的亮光无长突细胞.pdfVIP

Tetrodotoxin-Resistant Sodium Channels Contribute to Directional Responses in Starburst Amacrine Cells 1 2 Nicholas W. Oesch *, W. Rowland Taylor 1 Neuroscience Graduate Program, Oregon Health and Sciences University, Portland, Oregon, United States of America, 2 Casey Eye Institute, Oregon Health and Sciences University, Portland, Oregon, United States of America Abstract The biophysical mechanisms that give rise to direction selectivity in the retina remain uncertain. Current evidence suggests that the directional signal first arises within the dendrites of starburst amacrine cells (SBACs). Two models have been proposed to explain this phenomenon, one based on mutual inhibitory interactions between SBACs, and the other positing an intrinsic dendritic mechanism requiring a voltage-gradient depolarizing towards the dendritic tips. We tested these models by recording current and voltage responses to visual stimuli in SBACs. In agreement with previous work, we found that the excitatory currents in the SBACs were directional, and remained directional when GABA receptors were blocked. Contrary to the mutual-inhibitory model, stimuli that produce strong directional signals in ganglion cells failed to reveal a significant inhibitory input to SBACs. Suppression of the tonic excitatory conductance, proposed to generate the dendritic voltage- gradient required for the dendrite autonomous model, failed to eliminate the directional signal in SBACs. However, selective block of tetrodotoxin-resistant sodium channels did reduce the strength of the directional excitatory signal in the SBACs. These results indicate that current models of direction-selectivity in the SBACs are inadequate, and suggest that voltage-gated excitatory channels, specifically tetrodotoxin-resistant sodium channels, are