Lithium alters mu-opioid receptor expression in the rat brain

Gandarias, Juan M.; I, Acebes; Echevarrı́a, Enrique; Vegas, Laura Pina; Abecia, Luis Carlos; Casis, Luı́s

doi:10.1016/s0304-3940(99)00944-1

Cited by 17 publications

(6 citation statements)

References 17 publications

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“…Also, it has been proposed that lithium exerts a different, biphasic effect on morphine-induced antinociception (Dehpour et al, 1994). Although the effects of lithium on pain perception are reported to be dose-and testdependent (de Gandarias et al, 2000;Dehpour et al, 1994;, we did not observe any analgesic or algesic effect of lithium with the dose selected for our experiments.…”

Section: Resultscontrasting

confidence: 62%

“…Although its mechanism(s) of action as a mood stabilizer remain uncertain, it has been reported that systemic lithium administration causes hyperalgesia ( Johnston and Westbrook, 2004;McNally and Westbrook, 1998;Wiertelak et al, 1994) and attenuation of morphine-induced antinociception (Dehpour et al, 1994; in rodents, mainly by interfering with phosphotidylinositol turnover. Moreover, the effects of acute and chronic lithium administration on pain perception and morphine-induced analgesia are reported to be test-and dose-dependent (de Gandarias et al, 2000;Dehpour et al, 1994;. Careful review of the earlier studies reveals that no attempt was made to explore potential administration-time-dependent aspects of the interaction between lithium and morphine.…”

Section: Introductionmentioning

confidence: 99%

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Temporal Variation in Drug Interaction Between Lithium and Morphine‐Induced Analgesia

Karakucuk

Yamanoglu

Demirel

et al. 2006

Chronobiology International

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The administration-time-dependent aspects of the drug interaction between lithium and morphine-induced analgesia were studied using the mouse hot-plate test at six different times of day, each scheduled at 4 h intervals. Lithium treatment alone, in doses of 1 to 10 mmol/kg administered intraperitoneally (i.p.) did not significantly alter test latencies compared to the corresponding clock-time in saline-injected controls. Basal pain sensitivity and morphine-induced antinociceptive activity displayed significant circadian rhythms as assessed by the hot-plate response latencies, with higher values occurring during the nocturnal activity than during the daytime rest span. Acute administration of lithium, in a dose of 3 mmol/kg, 30 min prior to morphine dosing did not influence morphine-induced analgesia compared to all the clock-time test-matched morphine groups, except the 9 HALO (Hours After Lights On) one. There was a prominent potentiation of the morphine-induced antinociception at this biological time during combined drug treatment. The latter finding demonstrates that administration-time-dependent differences in drug-drug interactions need to be considered in both experimental designs and clinical settings.

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Section: Resultscontrasting

confidence: 62%

Section: Introductionmentioning

confidence: 99%

Temporal Variation in Drug Interaction Between Lithium and Morphine‐Induced Analgesia

Karakucuk

Yamanoglu

Demirel

et al. 2006

Chronobiology International

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“…However, this study did show an increase in 3 H]DAMGO binding in BA24 from people with BP who did not died by suicide. Some caution is needed in the interpretation of this finding in BP because of the relatively small number of individuals making up this cohort, particularly given that lithium treatment has been shown to increase OPRM expression in rats [34]. Although this novel finding deserves further investigation, it was not pursued in this study as it was not central to investigating the interactions between suicide x psychiatric disease.…”

Section: Discussionmentioning

confidence: 99%

Mu opioid receptor availability in people with psychiatric disorders who died by suicide: a case control study

et al. 2012

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BackgroundMu opioid receptors have previously been shown to be altered in people with affective disorders who died as a result of suicide. We wished to determine whether these changes were more widespread and independent of psychiatric diagnoses.MethodsMu receptor levels were determined using [3 H]DAMGO binding in BA24 from 51 control subjects; 38 people with schizophrenia (12 suicides); 20 people with major depressive disorder (15 suicides); 13 people with bipolar disorder (5 suicides) and 9 people who had no history of psychiatric disorders but who died as a result of suicide. Mu receptor levels were further determined in BA9 and caudate-putamen from 38 people with schizophrenia and 20 control subjects using [3 H]DAMGO binding and, in all three regions, using Western blots. Data was analysed using one-way ANOVAs with Bonferroni’s Multiple Comparison Test or, where data either didn’t approximate to a binomial distribution or the sample size was too small to determine distribution, a Kruskal-Wallis test with Dunn’s Multiple Comparison Test.Results[3 H]DAMGO binding density was lower in people who had died as a result of suicide (p<0.01). People with schizophrenia who had died as a result of suicide had lower binding than control subjects (p<0.001), whilst people with bipolar disorder (non- suicide) had higher levels of binding (p<0.05). [3 H]DAMGO binding densities, but not mu protein levels, were significantly decreased in BA9 from people with schizophrenia who died as a result of suicide (p<0.01).ConclusionsOverall these data suggest that mu opioid receptor availability is decreased in the brains of people with schizophrenia who died as a result of suicide, which would be consistent with increased levels of endogenous ligands occupying these receptors.

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“…Karakucuk et al (2006) and Ma¨nnisto¨and Saarnivaara (1972) did not observe any change in hot-plate response latencies after acute and chronic lithium treatment, respectively, while Dehpour et al (1994) reported a dosedependent biphasic effect in mice with chronic lithium administration. The mechanism of how lithium affects the analgesic response of morphine is not clear yet and several mechanisms have been hypothesized as changing the activity of the phosphoinositide pathway , reduction in cyclic AMP formation (Newman and Belmaker 1987), changes in the release of endogenous opioid peptides (Sivam et al 1988;Burns et al 1990) and increase in m-receptor density in rat brain (de Gandarias et al 2000).…”

Section: Biological Rhythm Research 363mentioning

confidence: 99%

The circadian rhythm of morphine-induced analgesia abolishes after chronic lithium treatment in old mice

Vural

Zengil

2009

Biological Rhythm Research

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The effect of chronic lithium treatment on morphine-induced analgesia was studied in a time-dependent manner in old mice. All mice received lithium chloride via drinking water of 600 mg/l for three weeks. Both basal pain sensitivity and morphine-induced analgesia were determined with a hot-plate test before and after chronic lithium drinking at six different times of the day every four hours. Chronic lithium exposure did not cause any significant change in basal pain sensitivity but the circadian rhythm of morphine analgesia disappeared in old mice. These findings suggest that biological rhythms may alter pharmacokinetic and pharmacodynamic properties of drugs and conversely drugs may alter the rhythmic properties of biological functions. Thus, administration time of drugs should be considered in both experimental designs and clinical settings.

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Lithium alters mu-opioid receptor expression in the rat brain

Cited by 17 publications

References 17 publications

Temporal Variation in Drug Interaction Between Lithium and Morphine‐Induced Analgesia

Temporal Variation in Drug Interaction Between Lithium and Morphine‐Induced Analgesia

Mu opioid receptor availability in people with psychiatric disorders who died by suicide: a case control study

The circadian rhythm of morphine-induced analgesia abolishes after chronic lithium treatment in old mice

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