Department of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, 1000 Wall Street, Ann Arbor, MI 48105, USA.
Neuron. 2011 Jul 14;71(1):166-79. doi: 10.1016/j.neuron.2011.04.033.
Retinal ganglion cells adapt by reducing their sensitivity during periods of high contrast. Contrast adaptation in the firing response depends on both presynaptic and intrinsic mechanisms. Here, we investigated intrinsic mechanisms for contrast adaptation in OFF Alpha ganglion cells in the in vitro guinea pig retina. Using either visual stimulation or current injection, we show that brief depolarization evoked spiking and suppressed firing during subsequent depolarization. The suppression could be explained by Na channel inactivation, as shown in salamander cells. However, brief hyperpolarization in the physiological range (5-10 mV) also suppressed firing during subsequent depolarization. This suppression was selectively sensitive to blockers of delayed-rectifier K channels (K(DR)). In somatic membrane patches, we observed tetraethylammonium-sensitive K(DR) currents that activated near -25 mV. Recovery from inactivation occurred at potentials hyperpolarized to V(rest). Brief periods of hyperpolarization apparently remove K(DR) inactivation and thereby increase the channel pool available to suppress excitability during subsequent depolarization.
视网膜神经节细胞通过在高对比度期间降低其敏感性来适应。在放电反应中的对比度适应取决于突触前和内在机制。在这里，我们研究了体外豚鼠视网膜中 OFF Alpha 神经节细胞的内在对比度适应机制。使用视觉刺激或电流注射，我们发现短暂去极化会引发放电，并在随后的去极化期间抑制放电。这种抑制可以通过 Na 通道失活来解释，就像在蝾螈细胞中一样。然而，在生理范围内（5-10 mV）的短暂超极化也会在随后的去极化期间抑制放电。这种抑制对延迟整流钾通道（K(DR)）的阻滞剂具有选择性敏感性。在体膜斑片上，我们观察到在接近-25 mV 时激活的四乙铵敏感的 K(DR)电流。失活的恢复发生在超极化到 V(rest)的电位。短暂的超极化期显然会消除 K(DR)失活，从而增加通道库，以便在随后的去极化期间抑制兴奋性。
