Wang Y, Harsanyi K, Mangel S C
Department of Neurobiology, University of Alabama School of Medicine, Birmingham 35294, USA.
J Neurophysiol. 1997 Jul;78(1):439-49. doi: 10.1152/jn.1997.78.1.439.
In the fish retina, horizontal cell electrical coupling and light responsiveness is regulated by activation of dopamine D1 receptors that are located on the horizontal cells themselves. The effects of dopamine and dopamine D2 receptor agonists and antagonists on cone horizontal cell light responses were studied in in vitro superfused goldfish retinas. Horizontal cell light responses and electrical coupling were assessed by monitoring responses to full-field stimuli and to small, centered (0.4 mm diam) spots of light, respectively. Dopamine (0.2-10 microM) application uncoupled horizontal cells and decreased their responses to full-field stimuli. Application of the D2 antagonist eticlopride (10-50 microM) produced similar effects, whereas quinpirole (0.1-10 microM), a D2 agonist, had the opposite effects. The uncoupling effect of eticlopride was blocked by prior application of SCH23390 (10 microM), a D1 receptor antagonist, and was eliminated after destruction of dopaminergic neurons by prior treatment of the retinas with 6-hydroxydopamine. The effects of these D2 drugs were observed following flickering light stimulation, but were not observed following sustained light stimulation. Application of the D2 antagonists sulpiride (0.5-20 microM) and spiperone (0.25-10 microM) uncoupled horizontal cells when the total concentration of divalent cations (Mg2+ and Ca2+) in the Ringer solution was 1.1 mM. However, when the concentration of divalent cations was 0.2 mM, spiperone had no effect on the horizontal cells and sulpiride increased coupling. In contrast, eticlopride uncoupled the cells and decreased their light responsiveness irrespective of the concentration of divalent cations. The effects of quinpirole also depended on the concentration of divalent cations; its coupling effect was reduced when the divalent cation concentration was increased from 0.2 to 1.0 mM. The results suggest that activation of D2 receptors in the fish retina by endogenous dopamine decreases dopamine release and is greater after flickering compared with sustained light stimulation. These D2 receptors thus function as presynaptic autoreceptors that inhibit dopamine release from dopaminergic cells. In addition, the results also indicate that the effectiveness of some D2 drugs at these receptors is dependent on the concentration of divalent cations.
在鱼类视网膜中，水平细胞的电耦合和光反应性受位于水平细胞自身上的多巴胺D1受体激活的调节。在体外灌注的金鱼视网膜中研究了多巴胺、多巴胺D2受体激动剂和拮抗剂对锥状水平细胞光反应的影响。分别通过监测对全场刺激和小的、位于中心的（直径0.4毫米）光点的反应来评估水平细胞的光反应和电耦合。施加多巴胺（0.2 - 10微摩尔）会使水平细胞解耦联，并降低它们对全场刺激的反应。施加D2拮抗剂依托必利（10 - 50微摩尔）产生类似的效果，而D2激动剂喹吡罗（0.1 - 10微摩尔）则产生相反的效果。依托必利的解耦联作用被预先施加的D1受体拮抗剂SCH23390（10微摩尔）阻断，并且在用6 - 羟基多巴胺预先处理视网膜破坏多巴胺能神经元后消除。这些D2药物的作用在闪烁光刺激后观察到，但在持续光刺激后未观察到。当林格溶液中二价阳离子（Mg2 +和Ca2 +）的总浓度为1.1毫摩尔时，施加D2拮抗剂舒必利（0.5 - 20微摩尔）和螺哌隆（0.25 - 10微摩尔）会使水平细胞解耦联。然而，当二价阳离子浓度为0.2毫摩尔时，螺哌隆对水平细胞没有影响，舒必利增加耦合。相比之下，无论二价阳离子浓度如何，依托必利都会使细胞解耦联并降低它们的光反应性。喹吡罗的作用也取决于二价阳离子的浓度；当二价阳离子浓度从0.2毫摩尔增加到1.0毫摩尔时，其耦合作用降低。结果表明，内源性多巴胺对鱼类视网膜中D2受体的激活会减少多巴胺释放，并且与持续光刺激相比，闪烁后更大。因此，这些D2受体作为突触前自身受体发挥作用，抑制多巴胺能细胞释放多巴胺。此外，结果还表明，一些D2药物在这些受体上的有效性取决于二价阳离子的浓度。
