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Endogenous opiates in the nucleus tractus solitarius mediate electroacupuncture-induced sleep activities in rats.

Cheng CH, Yi PL, Lin JG, Chang FC - Evid Based Complement Alternat Med (2011)

Bottom Line: 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 the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-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.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, Taipei 106, Taiwan.

ABSTRACT
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 the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-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 of β-endorphin and the involvement of the μ-opioid receptors.

No MeSH data available.


Related in: MedlinePlus

The effects of scopolamine on the 10 Hz EA stimuli-induced increase of β-endorphin. The 10 Hz EA stimuli significantly increased the expressions of β-endorphin in the brainstem and hippocampus and administration of scopolamine blocked EA-induced increases of β-endorphin concentration. *Represents a statistically significant difference between the values obtained from ipketamine + PFS + EA and ipketamine + PFS + sham EA. #Depicts a statistically significant difference between the values obtained from ipketamine + scopolamine + EA and ipketamine + PFS + EA.
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fig4: The effects of scopolamine on the 10 Hz EA stimuli-induced increase of β-endorphin. The 10 Hz EA stimuli significantly increased the expressions of β-endorphin in the brainstem and hippocampus and administration of scopolamine blocked EA-induced increases of β-endorphin concentration. *Represents a statistically significant difference between the values obtained from ipketamine + PFS + EA and ipketamine + PFS + sham EA. #Depicts a statistically significant difference between the values obtained from ipketamine + scopolamine + EA and ipketamine + PFS + EA.

Mentions: Our result demonstrated that delivery of sham EA stimuli did not alter the concentrations of β-endorphin within five distinct brain structures, including the brainstem, hypothalamus, cortex, hippocampus and striatum (Figure 4). However, application of EA stimuli at Anmian (EX17) acupoints for 20 min significantly enhanced the levels of β-endorphin in the brainstem and hippocampus, but not in the cortex, hypothalamus and striatum (Figure 4). Administration of the muscarinic receptor antagonist scopolamine directly into the NTS before the EA stimuli blocked EA-induced increases of β-endorphin in the brainstem and hippocampus (Figure 4).


Endogenous opiates in the nucleus tractus solitarius mediate electroacupuncture-induced sleep activities in rats.

Cheng CH, Yi PL, Lin JG, Chang FC - Evid Based Complement Alternat Med (2011)

The effects of scopolamine on the 10 Hz EA stimuli-induced increase of β-endorphin. The 10 Hz EA stimuli significantly increased the expressions of β-endorphin in the brainstem and hippocampus and administration of scopolamine blocked EA-induced increases of β-endorphin concentration. *Represents a statistically significant difference between the values obtained from ipketamine + PFS + EA and ipketamine + PFS + sham EA. #Depicts a statistically significant difference between the values obtained from ipketamine + scopolamine + EA and ipketamine + PFS + EA.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3094708&req=5

fig4: The effects of scopolamine on the 10 Hz EA stimuli-induced increase of β-endorphin. The 10 Hz EA stimuli significantly increased the expressions of β-endorphin in the brainstem and hippocampus and administration of scopolamine blocked EA-induced increases of β-endorphin concentration. *Represents a statistically significant difference between the values obtained from ipketamine + PFS + EA and ipketamine + PFS + sham EA. #Depicts a statistically significant difference between the values obtained from ipketamine + scopolamine + EA and ipketamine + PFS + EA.
Mentions: Our result demonstrated that delivery of sham EA stimuli did not alter the concentrations of β-endorphin within five distinct brain structures, including the brainstem, hypothalamus, cortex, hippocampus and striatum (Figure 4). However, application of EA stimuli at Anmian (EX17) acupoints for 20 min significantly enhanced the levels of β-endorphin in the brainstem and hippocampus, but not in the cortex, hypothalamus and striatum (Figure 4). Administration of the muscarinic receptor antagonist scopolamine directly into the NTS before the EA stimuli blocked EA-induced increases of β-endorphin in the brainstem and hippocampus (Figure 4).

Bottom Line: 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 the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-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.

View Article: PubMed Central - PubMed

Affiliation: Department of Veterinary Medicine, School of Veterinary Medicine, National Taiwan University, Taipei 106, Taiwan.

ABSTRACT
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 the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-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 of β-endorphin and the involvement of the μ-opioid receptors.

No MeSH data available.


Related in: MedlinePlus