Grassi Zucconi Gigliola, Cipriani Sabrina, Balgkouranidou Ioanna, Scattoni Roberto
Department of Cellular and Environmental Biology, University of Perugia, Perugia, Italy.
Brain Res Bull. 2006 Apr 28;69(4):375-81. doi: 10.1016/j.brainresbull.2006.01.009. Epub 2006 Feb 10.
Neurogenesis in the adult hippocampus can be up- or downregulated in response to a variety of physiological and pathological conditions. Among these, dysregulation of hippocampal neurogenesis has been recently implicated in the pathogenesis of depression. In addition, in animal models of depression, a variety of antidepressant treatments reverse that condition by increasing neurogenesis. As one night sleep deprivation is known to improve mood in depressed patients for at least 1 day, we investigated whether a comparable treatment may affect hippocampal neurogenesis in adult rats. Accordingly, rats were sleep-deprived by gentle handling for 12 h during their physiological period of rest, and were injected with bromodeoxyuridine 4 h and 2 h before the end of sleep deprivation. They were then perfused immediately thereafter, or after 15 days and 30 days. We found that 12 h sleep deprivation significantly increased cell proliferation and the total number of surviving cells in the hippocampal dentate gyrus soon after sleep deprivation, as well as 15 days and 30 days later, in comparison to control rats allowed to sleep. No changes were instead found in the subventricular zone of the lateral ventricles, indicating that 12 h sleep deprivation selectively triggers neurogenic signals to the hippocampus. The present data include acute sleep deprivation among the conditions which upregulate hippocampal neurogenesis and raise the possibility that such response could be implicated in the beneficial effects elicited in depressed patients by one night sleep deprivation. Thus, the findings could contribute to the understanding of the intriguing relationship between depression and neurogenesis in the adult brain.
成体海马体中的神经发生可根据多种生理和病理状况上调或下调。其中，海马体神经发生的失调最近被认为与抑郁症的发病机制有关。此外，在抑郁症动物模型中，多种抗抑郁治疗通过增加神经发生来逆转这种状况。由于已知一夜睡眠剥夺可使抑郁症患者的情绪至少在1天内得到改善，我们研究了类似的治疗是否会影响成年大鼠的海马体神经发生。因此，在大鼠的生理休息期通过轻柔处理使其睡眠剥夺12小时，并在睡眠剥夺结束前4小时和2小时注射溴脱氧尿苷。然后在之后立即、15天和30天后对它们进行灌注。我们发现，与允许睡眠的对照大鼠相比，12小时睡眠剥夺在睡眠剥夺后不久以及15天和30天后显著增加了海马齿状回中的细胞增殖和存活细胞总数。相反，在侧脑室的室下区未发现变化，这表明12小时睡眠剥夺选择性地触发了向海马体的神经发生信号。目前的数据表明，急性睡眠剥夺属于上调海马体神经发生的状况，并增加了这种反应可能与一夜睡眠剥夺对抑郁症患者产生的有益作用有关的可能性。因此，这些发现可能有助于理解成年大脑中抑郁症与神经发生之间的有趣关系。
