Voltage-gated Na channels in AII amacrine cells accelerate scotopic light responses mediated by the rod bipolar cell pathway.
Voltage-gated Na channels in AII amacrine cells accelerate scotopic light responses mediated by the rod bipolar cell pathway.
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DOI：
10.1523/jneurosci.4212-09.2010
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发表时间：
2010-03-31
期刊：
影响因子：
--
通讯作者：
Singer JH
中科院分区：
文献类型：
--
作者：
Tian M;Jarsky T;Murphy GJ;Rieke F;Singer JH
During night (i.e., scotopic) vision in mammals, rod photoreceptor output is conveyed to ganglion cells (GCs), the output cells of the retina, by a specialized neural circuit comprising rod bipolar (RB) and AII amacrine cells. Here, we examined how intrinsic postsynaptic conductances in AIIs contribute to transmission of rod-derived signals. Using paired recordings from synaptically-coupled RBs and AIIs, we found that a voltage-gated Na conductance in AII amacrines accelerated excitatory postsynaptic potentials (EPSPs) arising from RB synaptic input. EPSPs also could be amplified by the Na conductance when AIIs were hyperpolarized below resting membrane potential, thereby increasing the availability of Na channels. AII amacrines are coupled electrically and coupled AII amacrines likely receive common input from individual RBs. Na channel-mediated effects on EPSPs, however, appeared to occur at the single-cell rather than the AII network level. By recording light-evoked synaptic currents from GCs, we determined that the Na channel-dependent acceleration, but not amplification, of RB output by AII amacrines is reflected in the dynamics of AII synaptic output to retinal ganglion cells: synaptic inputs to both ON and OFF GCs are slowed equivalently --though not attenuated in amplitude-- when Na channels in AIIs are blocked. Thus, during scotopic vision, Na conductances in AIIs serve to accelerate RB output.
