Krizaj D, Witkovsky P
Department of Ophthalmology, New York University Medical Center, NY 10016.
Brain Res. 1993 Nov 5;627(1):122-8. doi: 10.1016/0006-8993(93)90755-c.
Dopamine has been postulated to act as an intraretinal messenger for light adaptation by biasing retinal circuits to favor cone over rod inputs to second- and third-order neurons. As an experimental test, we studied the effects of dopamine and related ligands on rod to horizontal cell synaptic transfer. Rods and horizontal cells (HC) were recorded from simultaneously. Red and green light-emitting diodes were modulated sinusoidally in counterphase at 1 Hz and their relative intensities adjusted to elicit a rod null. Dark-adapted HC's also showed a null, but exposure to 0.5-1.0 microM dopamine, which corresponds to the endogenous levels, elicited a large imbalance in the HC response while the rod null was maintained. Similar effects were achieved with either a D1 dopamine agonist, SKF 38393 (20 microM) or a D2 dopamine agonist, quinpirole HCl (1 microM). Correspondingly, the frequency range over which the HC responded to red flickering lights increased very substantially. Exposure to a D2, but not a D1 dopamine agonist increased rod flicker, but not as dramatically as in the HC. These data indicate that the synaptic gains of rod and cone transmission to a second order retinal neuron are modifiable by endogenous levels of dopamine. Secondly, the bandpass of rod flicker is altered by dopamine, acting through a D2 dopamine receptor.
多巴胺被假定为视网膜内的一种信使,通过使视网膜回路偏向于有利于锥体细胞而非杆体细胞向二级和三级神经元的输入,从而参与光适应过程。作为一项实验测试,我们研究了多巴胺及相关配体对杆体细胞向水平细胞突触传递的影响。同时记录杆体细胞和水平细胞(HC)的活动。红色和绿色发光二极管以1Hz的频率进行反相正弦调制,并调整它们的相对强度以引发杆体细胞反应缺失。暗适应的水平细胞也呈现反应缺失,但暴露于0.5 - 1.0微摩尔的多巴胺(这与内源性水平相对应)时,在维持杆体细胞反应缺失的同时,会引发水平细胞反应的巨大失衡。使用D1多巴胺激动剂SKF 38393(20微摩尔)或D2多巴胺激动剂盐酸喹吡罗(1微摩尔)也能产生类似效果。相应地,水平细胞对红色闪烁光做出反应的频率范围大幅增加。暴露于D2多巴胺激动剂而非D1多巴胺激动剂会增加杆体细胞的闪烁反应,但不如在水平细胞中那么显著。这些数据表明,杆体细胞和锥体细胞向二级视网膜神经元的突触增益可被内源性多巴胺水平所改变。其次,多巴胺通过D2多巴胺受体起作用,改变了杆体细胞闪烁的带通特性。