دانلود مقاله ISI انگلیسی شماره 69537
ترجمه فارسی عنوان مقاله

استرس مزمن در هنگام اختلال تنزل پارادوکسیک، باعث افزایش پاسخ پارادوکسیک خواب می شود: ارتباط با سطح پلاکتین پلاسما و محتوای سروتونین مغز

عنوان انگلیسی
Chronic stress during paradoxical sleep deprivation increases paradoxical sleep rebound: Association with prolactin plasma levels and brain serotonin content
کد مقاله سال انتشار تعداد صفحات مقاله انگلیسی
69537 2008 14 صفحه PDF
منبع

Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)

Journal : Psychoneuroendocrinology, Volume 33, Issue 9, October 2008, Pages 1211–1224

ترجمه کلمات کلیدی
محرومیت خواب پارادوکسیک، استرس فتوشیک، هوموستاز خواب ضربان قلب، پرولاکتین، کورتیکواسترون، دوپامین، سروتونین
کلمات کلیدی انگلیسی
Paradoxical sleep deprivation; Footshock stress; Sleep homeostasis; Heart rate; Prolactin; Corticosterone; Dopamine; Serotonin

چکیده انگلیسی

Previous studies suggest that stress associated to sleep deprivation methods can affect the expression of sleep rebound. In order to examine this association and possible mechanisms, rats were exposed to footshock stress during or immediately after a 96-h period of paradoxical sleep deprivation (PSD) and their sleep and heart rate were recorded. Control rats (maintained in individual home cages) and paradoxical sleep-deprived (PS-deprived) rats were distributed in three conditions (1) no footshock – NF; (2) single footshock – SFS: one single footshock session at the end of the PSD period (6–8 shocks per minute; 100 ms; 2 mA; for 40 min); and (3) multiple footshock – MFS: footshock sessions with the same characteristics as described above, twice a day throughout PSD (at 7:00 h and 19:00 h) and one extra session before the recovery period. After PSD, animals were allowed to sleep freely for 72 h. Additional groups were sacrificed at the end of the sleep deprivation period for blood sampling (ACTH, corticosterone, prolactin and catecholamine levels) and brain harvesting (monoamines and metabolites). Neither SFS nor MFS produced significant alterations in the sleep patterns of control rats. All PS-deprived groups exhibited increased heart rate which could be explained by increased dopaminergic activity in the medulla. As expected, PS deprivation induced rebound of paradoxical sleep in the first day of recovery; however, PSD + MFS group showed the highest rebound (327.3% above the baseline). This group also showed intermediate levels of corticosterone and the highest levels of prolactin, which were positively correlated with the length of PS episodes. Moreover, paradoxical sleep deprivation resulted in elevation of the serotonergic turnover in the hypothalamus, which partly explained the hormonal results, and in the hippocampus, which appears to be related to adaptive responses to stress. The data are discussed in the realm of a prospective importance of paradoxical sleep for processing of traumatic events.