Morphine Effects on the Spontaneous Electroencephalogram in Polydrug Abusers: Correlations with Subjective Self-Reports

Phillips, Robert L.; Herning, Ronald I.; London, Edythe D.

doi:10.1038/npp.1994.19

Cited by 19 publications

(12 citation statements)

References 20 publications

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“…Third, different opioids such as morphine and fentanyl can produce markedly different EEG patterns. For instance, Phillips et al (1994) found that morphine primarily affected alpha-band but not delta-band activity in heroin abusers, whereas in the present study fentanyl primarily affected delta-band but not alpha-band activity.…”

Section: Discussioncontrasting

confidence: 36%

“…Morphine-like drugs can increase EEG power in the delta (0.35-3.5 Hz) and theta frequency range (3.5-8 Hz) or decrease power in the alpha-band range (8-13 Hz) in awake, opioid-abusing individuals (Fink et al, 1971;Phillips et al, 1994;Volavka et al, 1970). Experimenter-administered fentanyl and other short-acting mu-opioid analgesics primarily increase delta-band power in surgical patients (Bovill et al, 1983;Scott et al, 1991;Sebel et al, 1981;Wauquier et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

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Mu-opioid Self-Administration vs Passive Administration in Heroin Abusers Produces Differential EEG Activation

Greenwald

Roehrs

2004

Neuropsychopharmacol

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Psychoactive drug self-administration (SA) produces different neurobiological effects than passive administration (PA) in non-human animals; however, such consequences have never been examined in human drug abusers. The present study compared electroencephalographic (EEG) activation produced by intravenous PA and SA of the mu-opioid fentanyl in eight heroin-dependent, methadone-stabilized male participants. In phase 1, participants received cumulative PA of fentanyl (up to 1.5 mg/70 kg; session 1), then bolus PA of placebo and fentanyl 1.5 mg/70 kg (session 2). High-dose fentanyl significantly increased the amplitude of slow-frequency (delta-and theta-band) EEG activity. In phase 2, bolus fentanyl 1.5 mg/70 kg was available for SA, requiring the participant to complete 1500 responses, in each of two sessions after saline or naloxone pretreatment. Delta EEG peak amplitude increases were greater following fentanyl SA than fentanyl PA, primarily over the central midline region, and were attenuated by naloxone pretreatment. The EEG increase and its attenuation by naloxone agree with preclinical evidence and suggest that SA-related EEG responses were mediated by opioid receptors.

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Section: Discussioncontrasting

confidence: 36%

Section: Introductionmentioning

confidence: 99%

Mu-opioid Self-Administration vs Passive Administration in Heroin Abusers Produces Differential EEG Activation

Greenwald

Roehrs

2004

Neuropsychopharmacol

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“…These two affect processed EEG in the same way at these concentrations [24], thus excluding a major difference between drugs on monitoring and excluding a major impact on our results. Morphine infusion may also interfere with processed EEG [11,25,26]. However, the doses of morphine administrated were low and identical in the two study groups and were not modified during the study period.…”

Section: Limitations Of the Present Studymentioning

confidence: 99%

Evaluation of two processed EEG analyzers for assessment of sedation after coronary artery bypass grafting

2000

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“…Negative consequences of disrupted sleep include an enhanced sensitivity to pain (Onen et al, 2001a, Onen et al, 2001b, Kundermann et al, 2004, Roehrs et al, 2006 and deficits in daytime performance leading to an increased risk of accidents (reviewed in Durmer and Dinges, 2005). Opioids disrupt wakefulness by causing impaired cognitive and psychomotor function (Clemons et al, 1996, Sjogren, 1997 and by increasing slow frequencies in the cortical electroencephalogram (EEG) (Volavka et al, 1970, Sebel et al, 1981, Wauquier et al, 1984, Scott et al, 1991, Phillips et al, 1994, Greenwald and Roehrs, 2005. Preclinical studies also show that systemic opioid administration disrupts deep sleep, inhibits REM sleep, and slows the cortical EEG during wakefulness (Colasanti and Khazan, 1973, King et al, 1981, de Andres et al, 1984, MayoMichelson and Young, 1993, Arankowsky-Sandoval and Gold, 1995, Osman et al, 2005.…”

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confidence: 99%

Sleep and GABA levels in the oral part of rat pontine reticular formation are decreased by local and systemic administration of morphine

2007

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Morphine, a μ-opioid receptor agonist, is a commonly prescribed treatment for pain. Although highly efficacious, morphine has many unwanted side effects including disruption of sleep and obtundation of wakefulness. One mechanism by which morphine alters sleep and wakefulness may be by modulating GABAergic signaling in brain regions regulating arousal, including the oral pontine reticular formation (PnO). This study used in vivo microdialysis in unanesthetized Sprague-Dawley rat to test the hypothesis that μ-opioid receptors modulate PnO GABA levels. Validation of the high performance liquid chromatographic technique used to quantify GABA was obtained by dialyzing the PnO (n=4 rats) with the GABA reuptake inhibitor nipecotic acid (500 μM). Nipecotic acid caused a 185±20% increase in PnO GABA levels, confirming chromatographic detection of GABA and demonstrating the existence of functional GABA transporters in rat PnO. Morphine caused a concentration-dependent decrease in PnO GABA levels (n=25 rats). Coadministration of morphine (100 μM) with naloxone (1 μM), a μ-opioid receptor antagonist, blocked the morphine-induced decrease in PnO GABA levels (n=5 rats). These results show for the first time that μ-opioid receptors in rat PnO modulate GABA levels. A second group of rats (n=6) was used to test the hypothesis that systemically administered morphine also decreases PnO GABA levels. Intravenous morphine caused a significant (p<0.05) decrease (19%) in PnO GABA levels relative to control intravenous infusions of saline. Finally, microinjections followed by 2 h recordings of electroencephalogram and electromyogram tested the hypothesis that PnO morphine administration disrupts sleep (n=8 rats). Morphine significantly (p<0.05) increased the percent of time spent in wakefulness (65%) and significantly (p<0.05) decreased the percent of rapid eye movement (REM) sleep (-53%) and non-REM sleep (-69%). The neurochemical and behavioral data suggest that morphine may disrupt sleep, at least in part, by decreasing GABAergic transmission in the PnO. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Access Author ManuscriptNeuroscience. Author manuscript; available in PMC 2009 August 20. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author ManuscriptOpioids such as morphine, that exert their effects primarily via the μ-opioid receptor, are the most efficacious and widely prescribed treatments for pain (Yaksh, 1997, Nicholson, 2003. Unfortunately, opioids have numerous side effects including sleep disruption (Kay et al., 1969, Kay, 1975. In healthy human voluntee...

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Morphine Effects on the Spontaneous Electroencephalogram in Polydrug Abusers: Correlations with Subjective Self-Reports

Cited by 19 publications

References 20 publications

Mu-opioid Self-Administration vs Passive Administration in Heroin Abusers Produces Differential EEG Activation

Mu-opioid Self-Administration vs Passive Administration in Heroin Abusers Produces Differential EEG Activation

Evaluation of two processed EEG analyzers for assessment of sedation after coronary artery bypass grafting

Sleep and GABA levels in the oral part of rat pontine reticular formation are decreased by local and systemic administration of morphine

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