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首页> 外文期刊>The European Journal of Neuroscience >The serotonergic anxiolytic buspirone attenuates circadian responses to light
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The serotonergic anxiolytic buspirone attenuates circadian responses to light

机译：血清素能抗焦虑药丁螺环酮减弱了昼夜节律对光的反应

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摘要

Serotonergic drugs modify circadian responses to light, with agonists attenuating and some partial agonists or antagonists potentiating photic phase shifts. The anxiolytic buspirone is a 5-HT1A receptor partial agonist. Given that buspirone is used therapeutically to manage generalised anxiety disorder, it would be useful to understand if and how this drug may modify circadian responses to light, not only to help manage side effects, but also to examine its potential use as a chronobiotic. Here we examined behavioral and molecular responses to phase-shifting light in mice and hamsters treated with buspirone. Phase advances to late subjective night light pulses in hamsters and wildtype mice were significantly attenuated by buspirone. 5-HT1A receptor knockout mice exhibited potentiated photic phase shifts when pretreated with buspirone. In wildtype mice, the attenuated phase shifts were accompanied by increased cFos expression in the suprachiasmatic nucleus, whereas potentiated phase shifts in knockouts were accompanied by increased phosphorylation of extracellular signal-regulated kinase (ERK) and cyclic AMP response element-binding protein (CREB), and decreased cFos expression. Attenuated photic phase shifts in buspirone-treated hamsters were accompanied by decreased phosphorylation of ERK and CREB. Chronic buspirone treatment decreased the amplitude of wheel-running rhythms, lengthened the duration of the active phase and advanced the phase angle of entrainment. Buspirone administration at midday produced non-photic phase advances in wildtype but not 5-HT1A receptor knockout mice. These findings suggest that buspirone affected the circadian system in a manner similar to the 5-HT1A/7 agonist (+/-)-8-Hydroxy-2-dipropylaminotetralin hydrobromide, primarily through the 5-HT1A receptor, and suggest that therapeutic use of buspirone to manage anxiety may impact circadian function.
机译：血清素能药物可以改变昼夜节律对光的反应，激动剂减弱，部分激动剂或拮抗剂增强光相。抗焦虑药丁螺环酮是5-HT1A受体部分激动剂。鉴于丁螺环酮在治疗上用于治疗广泛性焦虑症，了解该药物是否以及如何改变昼夜节律对光的反应，不仅有助于管理副作用，而且还可以检查其作为生时药的用途。在这里，我们检查了行为和分子对相移光在丁螺环酮治疗的小鼠和仓鼠中的反应。丁螺环酮显着减弱了仓鼠和野生型小鼠中晚期主观夜间脉冲的相位。 5-HT1A受体基因敲除小鼠用丁螺环酮预处理时，表现出增强的光相移。在野生型小鼠中，减弱的相移伴随着视交叉上核中cFos表达的增加，而基因敲除中增强的相移伴随着细胞外信号调节激酶（ERK）和环AMP反应元件结合蛋白（CREB）的磷酸化增加。 ，并降低cFos表达。在丁螺环酮处理的仓鼠中，减弱的光相变伴随着ERK和CREB磷酸化的降低。慢性丁螺环酮治疗可降低轮转节奏的幅度，延长活动期的持续时间，并提高夹带的相位角。在中午给予丁螺环酮在野生型小鼠中产生非光合阶段的进展，但在5-HT1A受体敲除小鼠中却没有。这些发现表明，丁螺环酮主要通过5-HT1A受体，以与5-HT1A / 7激动剂（+/-）-8-羟基-2-二丙基氨基四氢呋喃氢溴酸盐相似的方式影响昼夜节律系统，并建议将其用于治疗丁螺环酮治疗焦虑症可能会影响昼夜节律功能。

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