scholarly journals Endogenous Opiates in the Nucleus Tractus Solitarius Mediate Electroacupuncture-Induced Sleep Activities in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Chiung-Hsiang Cheng ◽  
Pei-Lu Yi ◽  
Jaung-Geng Lin ◽  
Fang-Chia Chang
Keyword(s):  
Receptor Antagonist ◽  
Eye Movement ◽  
Opioid Receptor ◽  
Nucleus Tractus Solitarius ◽  
Dark Period ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Opioidergic System ◽  
Opioid Receptor Antagonist ◽  
Stimulation Of

Electroacupuncture (EA) possesses various therapeutic effects, including alleviation of pain, reduction of inflammation and improvement of sleep disturbance. The mechanisms of EA on sleep improvement, however, remain to be determined. It has been stated in ancient Chinese literature that the Anmian (EX17) acupoint is one of the trigger points that alleviates insomnia. We previously demonstrated that EA stimulation of Anmian acupoints in rats during the dark period enhances non-rapid eye movement (NREM) sleep, which involves the induction of cholinergic activity in the nucleus tractus solitarius (NTS). In addition to cholinergic activation of the NTS, activation of the endogenous opioidergic system may also be a mechanism by which acupuncture affects sleep. Therefore, this study was designed to investigate the involvement of the NTS opioidergic system in EA-induced alterations in sleep. Our present results indicate that EA of Anmian acupoints increased NREM sleep, but not rapid eye movement sleep, during the dark period in rats. This enhancement in NREM sleep was dose-dependently blocked by microinjection of opioid receptor antagonist, naloxone, and theμ-opioid receptor antagonist, naloxonazine, into the NTS; administrations ofδ-receptor antagonist, natrindole, and theκ-receptor antagonist,nor-binaltrophimine, however, did not affect EA-induced alterations in sleep. Furthermore,β-endorphin was significantly increased in both the brainstem and hippocampus after the EA stimuli, an effect blocked by administration of the muscarinic antagonist scopolamine into the NTS. Our findings suggest that mechanisms of EA-induced NREM sleep enhancement may be mediated, in part, by cholinergic activation, stimulation of the opiodergic neurons to increase the concentrations ofβ-endorphin and the involvement of theμ-opioid receptors.

Ventilatory pattern after hypoxic stimulation during wakefulness and NREM sleep

1993 ◽  
Vol 75 (1) ◽  
pp. 397-404 ◽  
Author(s):  
K. Gleeson ◽  
L. W. Sweer
Keyword(s):  
Eye Movement ◽  
Ventilatory Response ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Identical Stimulus ◽  
Discharge Mechanism ◽  
Ventilatory Pattern ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Stimulation Of

The ventilatory after-discharge mechanism (VAD) may stabilize ventilation (VE) after hyperventilation but has not been studied in detail in humans. Several studies conducted during wakefulness suggest that VAD is present, although none has been conducted during sleep, when disordered ventilation is most common. We conducted two experiments during wakefulness and non-rapid-eye-movement (NREM) sleep in 14 healthy young men to characterize the ventilatory response after termination of a 45- to 60-s 10–12% O2 hypoxic stimulus. Eight subjects had triplicate hypoxic trials terminated by 100% O2 during wakefulness and NREM sleep. Hypoxia caused a drop in arterial O2 saturation to 78.5 +/- 0.5%, an increase in VE of 4.4 +/- 0.6 l/min, and a decrease in end-tidal PCO2 of 4.4 +/- 0.4 Torr during wakefulness, with no significant differences during sleep. When the hypoxia was terminated with 100% O2, VE was variable within and between subjects during wakefulness. During sleep, all subjects developed hypopnea (VE < 67% baseline) with a mean decrease of 65.5 +/- 7.8% at the onset of hyperoxia (P < 0.05 compared with baseline VE). We hypothesized that this uniform decrease in VE might be due to the nonphysiological hyperoxia employed. We therefore studied six additional subjects, all during NREM sleep, with identical hypoxic stimulation of breathing terminated by 100% O2 or room air. We again found that termination of hypoxia with 100% O2 produced uniform hypoventilation. However, when the identical stimulus was terminated with room air, no hypoventilation occurred.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Manipulating neural activity and sleep-dependent memory consolidation

Neuroforum ◽  
2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Maryam Ghorbani ◽  
Lisa Marshall
Keyword(s):  
Eye Movement ◽  
Neural Activity ◽  
Memory Consolidation ◽  
Nrem Sleep ◽  
Neural Oscillations ◽  
Rapid Eye Movement ◽  
Hippocampus Dependent Memory

AbstractSleep contributes actively to the consolidation of many forms of memory. This review describes the neural oscillations of non-rapid eye movement (NREM) sleep, the structures underlying these oscillations and their relation to hippocampus-dependent memory consolidation. A main focus lies on the relation between inter- and intraregional interactions and their electrophysiological representation. Methods for modulating neural oscillations with the intent of affecting memory consolidation are presented.

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