Kamp C W, Morgan W W
Eur J Pharmacol. 1981 Jan 29;69(3):273-9. doi: 10.1016/0014-2999(81)90473-8.
Previous results provided evidence for an inhibitory GABAergic influence on the dopamine neurons of the rat retina, without proving that endogenous GABA physiologically regulates the activity of these cells. We injected picrotoxinin intraocularly to dark-adapted rats and measured retinal dopamine turnover. Dopamine was analyzed radioenzymatically, and the decline in dopamine after alpha-methyl-p-tyrosine was used as an index of dopamine turnover. Picrotoxinin significantly stimulated dopamine turnover (P less than 0.05). In similar experiments with light-exposed rats picrotoxinin slightly enhanced dopamine turnover beyond that produced by light alone. Intraocular bicuculline methiodide produced similar results in dark-adapted and also in light-exposed rats. These data suggest that endogenous GABA tonically inhibits the activity of the retinal dopamine neurons in the dark and that there may be some remaining GABA tone on these cells in the light-exposed rat. Atropine pretreatment did not affect the picrotoxinin-induced activation of retinal dopamine turnover which negates the involvement of a cholinergic interneuron.
先前的研究结果表明,大鼠视网膜中存在抑制性γ-氨基丁酸(GABA)能对多巴胺能神经元产生影响,但并未证明内源性GABA在生理上调节这些细胞的活性。我们将印防己毒素眼内注射给暗适应的大鼠,并测量视网膜多巴胺的更新率。采用放射酶法分析多巴胺,并将α-甲基对酪氨酸处理后多巴胺的下降作为多巴胺更新率的指标。印防己毒素显著刺激了多巴胺更新率(P<0.05)。在对光照大鼠进行的类似实验中,印防己毒素使多巴胺更新率的增加略高于单独光照所产生的增加。眼内注射甲磺酸荷包牡丹碱在暗适应和光照大鼠中均产生了类似结果。这些数据表明,内源性GABA在黑暗中对视网膜多巴胺能神经元的活性起持续性抑制作用,并且在光照大鼠中这些细胞上可能仍存在一定的GABA张力。阿托品预处理并不影响印防己毒素诱导的视网膜多巴胺更新率的激活,这排除了胆碱能中间神经元的参与。