Direct correlation between level of morphine and its biochemical effect on monoamine systems in mouse brain

Ito, Koichi; Shibanoki, Shinji; McGaugh, James L.

doi:10.1016/0006-2952(83)90468-9

Cited by 15 publications

(5 citation statements)

References 17 publications

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“…The interval between a drug and a subsequent saline session was 6–8 h when a drug session was conducted in the morning and was 16–18 h when a drug session was conducted in the afternoon. Because the biological half-life of morphine in mouse brain is estimated to be 1 h (Ishikawa et al 1983), the concentration remaining at 6–8 and 16–18 h would be about 1 and 0.01 percent of the original concentration, respectively. While these washout periods may be sufficient for the elimination of low to moderate doses of morphine (i.e., 0.1–10 mg/kg), concentrations of morphine 6–8 h after high doses (32 and 100 mg/kg) may be similar to those acutely produced by 100-fold lower, but still behaviorally active, doses (i.e., 0.32 and 1 mg/kg).…”

Section: Discussionmentioning

confidence: 99%

Morphine-induced conditioned place preference and effects of morphine pre-exposure in adolescent and adult male C57BL/6J mice

Koek

2014

Psychopharmacology

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Rationale Given the increasing abuse of prescription opioids, particularly in adolescents, surprisingly few preclinical studies have explored effects of opioids in adolescents (versus adults). Objectives This study compared the conditioned rewarding effects of morphine, without (experiment 1) and with morphine pre-exposure (experiment 2), in adolescent and adult male mice. Methods Experiment 1: on each of three consecutive days, one of the two conditioning sessions was preceded by an injection of a particular dose of morphine (0.1, 0.32, 1, 3.2, 10, 32, or 100 mg/kg, i.p.) and the other by saline; place preference was tested on day 4. Experiment 2: mice received once daily injections of saline or a particular dose of morphine (17.8 or 56 mg/kg) for 4 days, and 3 days later, place conditioning with morphine (0.32, 1, 3.2, or 10 mg/kg) began. Results In both experiments, morphine induced conditioned place preference along similar inverted U-shaped dose-response curves in adolescent and adult mice, with maximal effects between 0.32–10 mg/kg. Morphine pre-exposure did not sensitize morphine-induced conditioned place preference; instead, tolerance occurred, but only in adults. Adolescents were more sensitive than adults to morphine-induced locomotor stimulation. Response to novelty predicted the locomotor stimulating effects of morphine in adolescents, but not its rewarding effects. Conclusions The rewarding effects of morphine were similar in adolescent and adult mice, but showed differential tolerance after morphine pre-exposure. Adolescents were more sensitive than adults to the acute locomotor stimulating effects of morphine, consistent with dopamine systems involved in locomotor activity being overactive during adolescence.

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Section: Discussionmentioning

confidence: 99%

Morphine-induced conditioned place preference and effects of morphine pre-exposure in adolescent and adult male C57BL/6J mice

Koek

2014

Psychopharmacology

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“…Morphine acts primarly by increasing the release of monoamines in the brain [11], cocaine by blocking monoamines reuptake [12], and amphetamine both by releasing and preventing monoamines reuptake [13]. The modulatory role of glucocorticoids on monoamine function in the mouse brain [19,20] as well as the regulatory effect on the synthesis and metabolism of monoamines [18,41,42] may give some help in understanding our results suggesting that DEX may interact with monoamine system probably by modulating its activity.…”

Section: General Commentsmentioning

confidence: 95%

“…These three drugs, i.e., morphine, cocaine and amphetamine increase motor activity by acting on monoamine system with different mechanisms of action [9,[10][11][12][13][14]. Morphine acts primarly by increasing the release of monoamines in the brain [11], cocaine by blocking monoamines reuptake [12], and amphetamine both by releasing and preventing monoamines reuptake [13].…”

Section: General Commentsmentioning

confidence: 99%

“…Morphine acts primarly by increasing the release of monoamines in the brain [11], cocaine exerts its effect by blocking monoamines reuptake [12] and amphetamine acts both by releasing monoamines and by preventing their reuptake [13]. Furthermore, it has been demonstrated that morphine acts as a monoamines releaser in a manner different to amphetamine [14].…”

Section: Introductionmentioning

confidence: 99%

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Glucocorticoids Involvement in the Control of CNS Excitability

Capasso

2007

RPCN

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The effect of dexamethasone (DEX) and its interaction with psychostimulants agents (morphine, cocaine and amphetamine) has been studied on locomotor activity and straub reaction in mice: a) Morphine administration, (30-75-150 mg/kg,ip) induced a dose-related increase of the locomotor activity of mice, whereas DEX per se (0.1-1.0-10 mg/kg,ip) did not modify the activity of control mice. Pretreatment of mice with DEX 0.1 mg did not alter the hyperactivity produced by the three doses of morphine. In contrast, DEX administered at 1.0 mg reduced the morphine effects on locomotor activity, whereas DEX at 10 mg potentiated the morphine hypermotility. b) Cocaine (10 mg/kg/i.p.) and amphetamine (5 mg/kg/i.p.) increased markedly locomotor activity of mice whereas DEX per se (0.1-1.0-10 mg/kg/i.p.) did not modify the activity of control mice. DEX pretreatment decreased the stimulating effects induced by cocaine and amphetamine. DEX pretreatment 0, 15, 30, 60 and 120 min before amphetamine or cocaine strongly decreased both amphetamine and cocaine effects, but no dose-related effect was observed. The time-course study performed with DEX revealed differences in its reducing effect on cocaine and amphetamine hypermotility when the groups of animals treated with the steroid immediately before the cocaine (or amphetamine) injection when compared to those treated with the steroid later (15, 30, 60 and 120 min). Furthermore, actinomycin D was able to block the reducing effect of DEX on both amphetamine and cocaine hypermotility. c) When morphine was administered in doses of 7.5, 15 and 30 mg/kg/i.p, a dose-dependent straub reaction was produced. DEX per se (0.1-1.0-10 mg /kg,i.p.) did not modify the tail of control mice. Pre-treatment with DEX 120 min before morphine injection caused a dose-dependent reduction of straub reaction. Cycloheximide (15 mg/kg,i.p.) administered 2h before morphine did not change morphine-induced straub reaction, but was able to prevent the effects of DEX on morphine-induced straub reaction. The glucocorticoid receptor antagonist RU-38486 (15 mg/kg,i.p.) did not affect morphine-induced straub reaction, whereas it was able to block the effects of dexamethasone on morphine-induced straub reaction. Our results suggest that DEX may play an important regulatory role on the central effects of morphine, cocaine and amphetamine through a differential modulation of brain excitability systems indicating that DEX may play an important role on the stimulating effects of morphine, cocaine and amphetamine and that it may be of some utility in the clinical management of psychastimuants abuse. The ability of actinomicyn D and/or cycloheximide as well as of RU-38486 to block dexamethasone's effects indicates that the steroid's interference with psychostimulants-mediated effects involve a protein-synthesis-dependent mechanism via glucocorticoid receptors. The patents related to psychostimulant agent and glucocorticoids are also discussed in this article.

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“…There is evidence that opioids can modify several biochemical parameters that re¯ect presynaptic activity in dopaminergic neurons, such as the synthesis (Ishikawa et al, 1983;Spampinato et al, 1984) and release (Loh et al, 1976;Pollard et al, 1977;Walker et al, 1987;Werling et al, 1988;Heijna et al, 1990) of dopamine. Treatment with morphine is associated with the development of dopamine receptor supersensitivity (Iversen and Joyce, 1978;Ritzman et al, 1979;Bhargava, 1980;Martin and Takemori, 1986).…”

Section: Introductionmentioning

confidence: 97%

Comparison of the effect of levodopa and bromocriptine on naloxone-precipitated morphine withdrawal symptoms in mice

Samini

Fakhrian

Mohagheghi

et al. 2000

Hum. Psychopharmacol. Clin. Exp.

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In this study, the effect of l-dopa and bromocriptine on morphine withdrawal syndrome was compared. Both l-dopa (125, 250 mg/kg, i.p.) and low doses of bromocriptine (0.04, 0.08 mg/kg, i.p.) potentiated naloxone-induced morphine withdrawal symptoms such as jumping, climbing and rearing in mice. Higher doses of bromocriptine (0.16, 0.32 mg/kg, i.p.) attenuated these naloxone-induced symptoms. SKF 83566, D(1) dopamine antagonist (0.4, 0.8 mg/kg, i.p.) and sulpiride, D(2) dopamine antagonist (5, 10 mg/kg, i.p.) when used alone, also produced inhibitory effects on naloxone-induced morphine withdrawal symptoms. Pretreatment with sulpiride (5, 10 mg/kg, i.p.) and SKF 83566 (0.4, 0.8 mg/kg, i.p.) attenuated the potentiating effects of l-dopa on withdrawal symptoms significantly. Pretreatment with sulpiride also decreased the potentiating effect of bromocriptine and reinforced the inhibitory action of it, but SKF 83566 pretreatment just reinforced the effect of higher doses of bromocriptine. Concurrent pretreatment of animals with sulpiride (10 mg/kg, i.p.) and SKF 83566 (0.8 mg/kg, i.p.) markedly decreased the potentiating effects of l-dopa and bromocriptine and reinforced the inhibitory action of bromocriptine on the naloxone-induced morphine withdrawal syndrome. Prazosin, alpha(1) antagonist (1, 2 mg/kg, i.p.) decreased the naloxone-induced morphine withdrawal syndrome significantly. Pretreatment with yohimbine, alpha(2)-antagonist (5 mg/kg, i.p.) reversed the inhibitory effects of bromocriptine (0.16, 0.32 mg/kg, i.p.) on naloxone-induced morphine withdrawal syndrome significantly. In conclusion, our results show that bromocriptine at lower doses (0.04, 0.08 mg/kg, i.p.) acts similar to l-dopa, but at higher doses (0.16, 0.32 mg/kg, i.p.) shows different effects on naloxone-induced morphine withdrawal syndrome which may be due to the interaction of bromocriptine with alpha-adrenoceptors. Copyright 2000 John Wiley & Sons, Ltd.

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Direct correlation between level of morphine and its biochemical effect on monoamine systems in mouse brain

Cited by 15 publications

References 17 publications

Morphine-induced conditioned place preference and effects of morphine pre-exposure in adolescent and adult male C57BL/6J mice

Morphine-induced conditioned place preference and effects of morphine pre-exposure in adolescent and adult male C57BL/6J mice

Glucocorticoids Involvement in the Control of CNS Excitability

Comparison of the effect of levodopa and bromocriptine on naloxone-precipitated morphine withdrawal symptoms in mice

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