Presynaptic mechanism for slow contrast adaptation in mammalian retinal ganglion cells
Presynaptic mechanism for slow contrast adaptation in mammalian retinal ganglion cells
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DOI：
10.1016/j.neuron.2006.03.039
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发表时间：
2006-05-04
期刊：
影响因子：
16.2
通讯作者：
Demb, Jonathan B.
中科院分区：
文献类型：
--
作者：
Manookin, Michael B.;Demb, Jonathan B.
从视网膜到皮层的视觉神经元对刺激对比度的适应是缓慢的。在从高对比度切换到低对比度之后，神经元迅速降低其响应性并在5-20秒内恢复。皮质适应性来自一种内在的细胞机制：钠依赖性钾传导，导致延长的超极化。尖峰可以驱动这种机制，提高了视网膜神经节细胞中存在相同机制的可能性。我们发现，神经节细胞的适应对应于超极化后的缓慢恢复（AHP），但是，与皮质细胞不同，这种AHP主要不是由内在的细胞特性驱动的：尖峰不足以产生适应。适应是最强的空间刺激调谐到突触前双极细胞，而不是神经节细胞，它是由减少兴奋性电导驱动，并持续阻断GABA和甘氨酸受体，K-（Ca）通道或mGluRs。因此，缓慢的适应是由于突触前（非尖峰）双极细胞谷氨酸释放减少引起的。
Visual neurons, from retina to cortex, adapt slowly to stimulus contrast. Following a switch from high to low contrast, a neuron rapidly decreases its responsiveness and recovers over 5-20 s. Cortical adaptation arises from an intrinsic cellular mechanism: a sodium-dependent potassium conductance that causes prolonged hyperpolarization. Spiking can drive this mechanism, raising the possibility that the same mechanism exists in retinal ganglion cells. We found that adaptation in ganglion cells corresponds to a slowly recovering after hyperpolarization (AHP), but, unlike in cortical cells, this AHP is not primarily driven by an intrinsic cellular property: spiking was not sufficient to generate adaptation. Adaptation was strongest following spatial stimuli tuned to presynaptic bipolar cells rather than the ganglion cell; it was driven by a reduced excitatory conductance, and it persisted while blocking GABA and glycine receptors, K-(Ca) channels or mGluRs. Thus, slow adaptation arises from reduced glutamate release from presynaptic (nonspiking) bipolar cells.