Abstract：
BACKGROUND: Pituitary lactotrophs are under tonic dopaminergic inhibitory control and bromocriptine treatment blocks prolactin secretion.
METHODS: Sleep and local field potential were addressed for 72 h after bromocriptine treatments applied during the different stages of the estrus cycle and for 24 h in the early- and middle postpartum period characterized by spontaneously different dynamics of prolactin release in female rats.
RESULTS: Sleep changes showed strong dependency on the estrus cycle phase of the drug application. Strongest increase of wakefulness and reduction of slow wave sleep- and rapid eye movements sleep appeared during diestrus-proestrus and middle postpartum treatments. Stronger sleep-wake effects appeared in the dark phase in case of the estrus cycle treatments, but in the light phase in postpartum treatments. Slow wave sleep and REM sleep loss in case of estrus cycle treatments was not compensated at all and sleep loss seen in the first day post-injection was gained further later. In opposition, slow wave sleep loss in the light phase after bromocriptine injections showed compensation in the postpartum period treatments. Bromocriptine treatments resulted in a depression of local field potential delta power during slow wave sleep while an enhancement in beta and gamma power during wakefulness regardless of the treatment timing.
CONCLUSIONS: These results can be explained by the interplay of dopamine D2 receptor agonism, lack of prolactin release and the spontaneous homeostatic sleep drive being altered in the different stages of the estrus cycle and the postpartum period.
METHODS: Sleep and local field potential were addressed for 72 h after bromocriptine treatments applied during the different stages of the estrus cycle and for 24 h in the early- and middle postpartum period characterized by spontaneously different dynamics of prolactin release in female rats.
RESULTS: Sleep changes showed strong dependency on the estrus cycle phase of the drug application. Strongest increase of wakefulness and reduction of slow wave sleep- and rapid eye movements sleep appeared during diestrus-proestrus and middle postpartum treatments. Stronger sleep-wake effects appeared in the dark phase in case of the estrus cycle treatments, but in the light phase in postpartum treatments. Slow wave sleep and REM sleep loss in case of estrus cycle treatments was not compensated at all and sleep loss seen in the first day post-injection was gained further later. In opposition, slow wave sleep loss in the light phase after bromocriptine injections showed compensation in the postpartum period treatments. Bromocriptine treatments resulted in a depression of local field potential delta power during slow wave sleep while an enhancement in beta and gamma power during wakefulness regardless of the treatment timing.
CONCLUSIONS: These results can be explained by the interplay of dopamine D2 receptor agonism, lack of prolactin release and the spontaneous homeostatic sleep drive being altered in the different stages of the estrus cycle and the postpartum period.
摘要：
背景：垂体催乳菌处于强直多巴胺能抑制控制下，溴隐亭治疗阻断催乳素分泌。
方法：在发情周期的不同阶段应用溴隐亭治疗后72小时，在产后早期和中期进行24小时，以自发的不同动力学为特征雌性大鼠催乳素释放。
结果：睡眠变化对药物应用的发情周期有很强的依赖性。在发情期-发情期和产后中期治疗期间，觉醒的最大增加和慢波睡眠和快速眼动睡眠的减少。在发情周期治疗的情况下，在黑暗阶段出现更强的睡眠-觉醒效应，但在产后治疗中处于轻度阶段。在发情周期治疗的情况下，慢波睡眠和REM睡眠损失根本没有得到补偿，并且在注射后第一天看到的睡眠损失进一步增加。在反对中，溴隐亭注射后轻度阶段的慢波睡眠损失在产后治疗中显示出补偿。溴隐亭治疗导致慢波睡眠期间局部场电位δ功率降低，而无论治疗时机如何，觉醒期间β和γ功率均增强。
结论：这些结果可以通过多巴胺D2受体激动作用的相互作用来解释，在发情周期和产后的不同阶段，催乳素释放不足和自发的稳态睡眠驱动被改变。
方法：在发情周期的不同阶段应用溴隐亭治疗后72小时，在产后早期和中期进行24小时，以自发的不同动力学为特征雌性大鼠催乳素释放。
结果：睡眠变化对药物应用的发情周期有很强的依赖性。在发情期-发情期和产后中期治疗期间，觉醒的最大增加和慢波睡眠和快速眼动睡眠的减少。在发情周期治疗的情况下，在黑暗阶段出现更强的睡眠-觉醒效应，但在产后治疗中处于轻度阶段。在发情周期治疗的情况下，慢波睡眠和REM睡眠损失根本没有得到补偿，并且在注射后第一天看到的睡眠损失进一步增加。在反对中，溴隐亭注射后轻度阶段的慢波睡眠损失在产后治疗中显示出补偿。溴隐亭治疗导致慢波睡眠期间局部场电位δ功率降低，而无论治疗时机如何，觉醒期间β和γ功率均增强。
结论：这些结果可以通过多巴胺D2受体激动作用的相互作用来解释，在发情周期和产后的不同阶段，催乳素释放不足和自发的稳态睡眠驱动被改变。
