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Journal of Zhejiang University SCIENCE B 1998 Vol.-1 No.-1 P.

http://doi.org/10.1631/jzus.B2400048


Competitive roles of SO/delta-nesting-mediated sleep disruption under acute methamphetamine exposure in monkeys


Author(s):  Xin LV, Jie LIU, Shuo MA, Yuhan WANG, Yixin PAN, Xian QIU, Bomin SUN, Shikun ZHAN

Affiliation(s):  Department of Functional Neurosurgery, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China

Corresponding email(s):   shikun_zhan@hotmail.com, sbm11224@rjh.com.cn

Key Words:  Amphetamine, Sleep stage, Slow oscillation, Delta oscillation, Addiction, EEG


Xin LV, Jie LIU, Shuo MA, Yuhan WANG, Yixin PAN, Xian QIU, Bomin SUN, Shikun ZHAN. Competitive roles of SO/delta-nesting-mediated sleep disruption under acute methamphetamine exposure in monkeys[J]. Journal of Zhejiang University Science B, 1998, -1(-1): .

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Abstract: 
Abuse of amphetamine-based stimulants is a primary public health concern. Recent studies have underscored a troubling escalation in the inappropriate use of prescription amphetamine-based stimulants. However, the neurophysiological mechanisms underlying the impact of acute methamphetamine exposure (AME) on sleep homeostasis remain to be explored. This study employed non-human primates and electroencephalogram (EEG) sleep staging to evaluate the influence of AME on neural oscillations. The primary focus was on alterations in spindles, delta oscillations, and slow oscillations (SO), and their interactions as conduits through which AME influences sleep stability. AME predominantly diminishes sleep-spindle waves in the non-rapid-eye-movement 2 (NREM2) stage, and impacts slow oscillations and delta waves differentially. Furthermore, the competitive relationships between SO/delta waves nesting with sleep spindles were selectively strengthened by methamphetamine. Complexity analysis also revealed that the SO-nested spindles had lost their function of maintaining sleep depth and sleep stability. In summary, this finding could be one of the intrinsic electrophysiological mechanisms by which AME leads to disruption of sleep homeostasis.

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