Manookin Michael B, Demb Jonathan B
Neuroscience Program, University of Michigan, Ann Arbor, Michigan 48105, USA.
Neuron. 2006 May 4;50(3):453-64. doi: 10.1016/j.neuron.2006.03.039.
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 afterhyperpolarization (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.
从视网膜到皮层的视觉神经元对刺激对比度适应缓慢。从高对比度切换到低对比度后，神经元会迅速降低其反应性，并在5 - 20秒内恢复。皮层适应源于一种内在的细胞机制：一种依赖钠的钾电导，它会导致长时间的超极化。发放冲动可以驱动这种机制，这增加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中的适应对应于一个恢复缓慢的后超极化（AHP），但是，与皮层细胞不同的是，这种AHP并非主要由内在细胞特性驱动：发放冲动不足以产生适应。在针对突触前双极细胞而非神经节细胞进行调谐的空间刺激后，适应最为强烈；它是由兴奋性电导降低所驱动的，并且在阻断GABA和甘氨酸受体、K（Ca）通道或代谢型谷氨酸受体时仍然持续存在。因此，缓慢适应源于突触前（非发放冲动的）双极细胞谷氨酸释放的减少。
