Bui Bang V, Fortune Brad
Discoveries in Sight, Devers Eye Institute, Legacy Health System, Portland, Oregon 97232, USA.
Vis Neurosci. 2006 Mar-Apr;23(2):155-67. doi: 10.1017/S0952523806232024.
We assessed the growth of the rat photopic electroretinogram (ERG) during light adaptation and the mechanisms underlying this process. Full field ERG responses were recorded from anesthetized adult Brown-Norway rats at each minute for 20 min of light adaptation (backgrounds: 1.8, 2.1, 2.4 log scotopic cd m(-2)). The rat photopic b-wave amplitude increased with duration of light adaptation and its width at 33% maximal amplitude narrowed (by approximately 40 ms). These effects peaked 12-15 min after background onset. The narrowing of the b-wave reflected steepening of the b-wave recovery phase, with little change in the rising phase. OP amplitudes grew in proportion to the b-wave. Inhibition of inner retinal responses using TTX resulted in a greater relative growth of b-wave and OP amplitude compared with fellow control eyes, and delayed the change in recovery phase by approximately 5 min. Inhibition of all ionotropic glutamate receptors with CNQX/D-AP7 delayed both rising and recovery phases equally (approximately 12 ms) without altering b-wave width or the time course of adaptation changes. These outcomes suggest that inner retinal light responses are not directly responsible for b-wave amplitude growth, but may contribute to the change in its recovery phase during adaptation. A TTX-sensitive mechanism may help to hasten this process. The cone a-wave was isolated using PDA/L-AP4 or CNQX/L-AP4. A-wave amplitude (35 ms after stimulus onset) also increased with time during light adaptation and reached a maximum (130 +/- 29% above baseline) 12-15 min after background onset. B-wave amplitude growth in fellow control eyes closely followed the course and relative magnitude of cone a-wave amplitude growth. Hence, the increase of the cone response during light adaptation is sufficient to explain b-wave amplitude growth.
我们评估了大鼠明视视网膜电图(ERG)在光适应过程中的增长情况以及该过程的潜在机制。在光适应20分钟期间(背景:1.8、2.1、2.4 log暗视cd m(-2)),每分钟从麻醉的成年棕色挪威大鼠记录全视野ERG反应。大鼠明视b波振幅随光适应持续时间增加,其在最大振幅33%处的宽度变窄(约40毫秒)。这些效应在背景开始后12 - 15分钟达到峰值。b波变窄反映了b波恢复相的变陡,上升相变化不大。OP振幅与b波成比例增长。使用TTX抑制视网膜内层反应导致与对照眼相比,b波和OP振幅有更大的相对增长,并使恢复相的变化延迟约5分钟。用CNQX/D - AP7抑制所有离子型谷氨酸受体使上升相和恢复相同样延迟(约12毫秒),而不改变b波宽度或适应变化的时间进程。这些结果表明,视网膜内层光反应并非b波振幅增长的直接原因,但可能有助于其在适应过程中恢复相的变化。一种对TTX敏感的机制可能有助于加速这一过程。使用PDA/L - AP4或CNQX/L - AP4分离出视锥a波。光适应期间,刺激开始后35毫秒时的a波振幅也随时间增加,并在背景开始后12 - 15分钟达到最大值(比基线高130±29%)。对照眼的b波振幅增长紧密跟随视锥a波振幅增长的过程和相对幅度。因此,光适应期间视锥反应的增加足以解释b波振幅的增长。