Keefe D L, Earnest D J, Nelson D, Takahashi J S, Turek F W
Brain Res. 1987 Feb 17;403(2):308-12. doi: 10.1016/0006-8993(87)90068-0.
Despite the well known role of the light-dark cycle in the entrainment of circadian rhythms, very little is known about the neurochemical events that mediate the effects of light on the mammalian circadian clock. Recent anatomical and pharmacological data support the hypothesis that acetylcholine may be involved in relaying light-dark information from the retina to, or within, the circadian clock of rodents. If acetylcholine is required for this response, it should be possible to block the phase-shifting effects of a light pulse by blocking cholinergic neurotransmission. To test this possibility, hamsters free-running in constant darkness received an intraventricular injection of the anticholinergic drug, mecamylamine (450 micrograms), 10 min before being exposed to a 5-min pulse of light known to induce sub-maximal phase shifts in the circadian rhythm of wheel-running behavior. Compared to vehicle-injected control animals, mecamylamine treatment blocked or reduced both the phase-advancing and phase-delaying effects of light. These results support the hypothesis that acetylcholine is involved in mediating the phase-shifting effects of light on the mammalian circadian clock.
尽管明暗周期在昼夜节律的同步化中所起的作用广为人知，但对于介导光对哺乳动物生物钟影响的神经化学事件却知之甚少。最近的解剖学和药理学数据支持这样一种假说，即乙酰胆碱可能参与将明暗信息从视网膜传递至啮齿动物的生物钟或在生物钟内部进行传递。如果这种反应需要乙酰胆碱，那么通过阻断胆碱能神经传递应该能够阻断光脉冲的相位移动效应。为了验证这种可能性，在持续黑暗中自由活动的仓鼠在暴露于已知能在昼夜节律的轮转行为中诱导次最大相位移动的5分钟光脉冲前10分钟，接受了脑室注射抗胆碱能药物美加明（450微克）。与注射赋形剂的对照动物相比，美加明处理阻断或降低了光的相位提前和相位延迟效应。这些结果支持了乙酰胆碱参与介导光对哺乳动物生物钟的相位移动效应这一假说。
