Coadministration of dextromethorphan during pregnancy and throughout lactation prevents morphine-induced hyperprolactinemia in female rats

Wu, Ling-Yi; Huang, Eagle Yi‐Kung; Tao, Pao‐Luh

doi:10.1016/j.fertnstert.2009.01.143

Cited by 7 publications

(3 citation statements)

References 52 publications

(53 reference statements)

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“…The current results implied the possible biological change in offspring from morphine-addicted mother in humans. Moreover, the therapeutic potential of DM was further highlighted; especially our previous report also indicated the ability of DM to reduce morphine-induced hyperprolactinemia in female rats at different reproductive stages [27]. …”

Section: Discussionmentioning

confidence: 99%

Attenuation by dextromethorphan on the higher liability to morphine-induced reward, caused by prenatal exposure of morphine in rat offspring

Chen

Tao

et al. 2009

J Biomed Sci

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Co-administration of dextromethorphan (DM) with morphine during pregnancy and throughout lactation has been found to reduce morphine physical dependence and tolerance in rat offspring. No evidence was presented, however, for the effect of DM co-administered with morphine during pregnancy on morphine-induced reward and behavioral sensitization (possibly related to the potential to induce morphine addiction) in morphine-exposed offspring. Conditioned place preference and locomotor activity tests revealed that the p60 male offspring of chronic morphine-treated female rats were more vulnerable to morphine-induced reward and behavioral sensitization. The administration of a low dose of morphine (1 mg/kg, i.p.) in these male offspring also increased the dopamine and serotonin turnover rates in the nucleus accumbens, which implied that they were more sensitive to morphine. Co-administration of DM with morphine in the dams prevented this adverse effect of morphine in the offspring rats. Thus, DM may possibly have a great potential in the prevention of higher vulnerability to psychological dependence of morphine in the offspring of morphine-addicted mothers.

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Section: Discussionmentioning

confidence: 99%

Attenuation by dextromethorphan on the higher liability to morphine-induced reward, caused by prenatal exposure of morphine in rat offspring

Chen

Tao

et al. 2009

J Biomed Sci

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“…Studies have shown that DM reduced morphine reward as measured by CPP test, and this might be related to DM’s antagonizing effect on NMDA receptors that are involved in the activation of mesocorticolimbic dopaminergic systems [ 25 , 26 ]. Our previous studies also demonstrated that co-administration of DM with morphine during pregnancy and throughout lactation reduced several morphine-induced adverse effects [ 27 , 28 ] and could prevent higher vulnerability to inflammatory thermal hyperalgesia in rat offspring [ 29 ].…”

Section: Introductionmentioning

confidence: 99%

Beneficial effects of co-treatment with dextromethorphan on prenatally methadone-exposed offspring

Chiang

Hsu

et al. 2015

J Biomed Sci

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BackgroundHeroin use among young women of reproductive age has drawn much attention around the world. Although methadone is widely used in maintenance therapy for heroin/morphine addiction, the long-term effects of prenatal exposure to methadone and preventative therapy remain unclear. For revealing this question, female pregnant Sprague–Dawley rats were sub-grouped to receive (1) vehicle, (2) methadone 5 mg/kg at embryonic day 3 (E3) and then 7 mg/kg from E4 to E20, (3) dextromethorphan (DM) 3 mg/kg, and (4) methadone + DM (the rats received methadone followed by DM treatment), subcutaneously, twice a day from E3 to E20. The body weight, natural withdrawal, pain sensitivity, ED50, conditioned place preference and water maze were conducted at different postnatal stages (P1 to P79) of offspring. The quantitative real-time RT-PCR and electrophysiology were also used to measure the gene expression of opioid receptors in the spinal cord and changes of LTP/LTD in the hippocampus, separately.ResultsPrenatal exposure to methadone or DM did not affect survival rate, body weight, water maze and LTP or LTD of offspring. However, prenatal methadone significantly increased the withdrawal symptoms, pain sensitivity, addiction liability and decreased the mRNA expression of pain related opioid receptors. Co-administration of DM with methadone in the maternal rats effectively prevented these abnormalities of offspring induced by methadone.ConclusionsOur study clearly showed that co-administration of dextromethorphan with methadone in the maternal rats prevented the adverse effects induced by prenatal methadone exposure. It implies that dextromethorphan may have a potential to be used in combination with methadone for maintenance treatment in pregnant heroin-addicted women to prevent the adverse effects induced by methadone on offspring.Electronic supplementary materialThe online version of this article (doi:10.1186/s12929-015-0126-2) contains supplementary material, which is available to authorized users.

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“…The current results also implied the possible biological change in the CNS of offspring from morphine-addicted mother in humans. Moreover, the therapeutic potential of DM was further highlighted; especially our recent report also indicated the ability of DM to reduce morphine-induced hyperprolactinemia in female rats at different reproductive stages [33]. …”

Section: Discussionmentioning

confidence: 99%

Dextromethorphan attenuated the higher vulnerability to inflammatory thermal hyperalgesia caused by prenatal morphine exposure in rat offspring

2011

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BackgroundCo-administration of dextromethorphan (DM) with morphine during pregnancy and throughout lactation has been found to reduce morphine physical dependence and tolerance in rat offspring. No evidence was presented, however, for the effect of DM co-administered with morphine during pregnancy on inflammatory hyperalgesia in morphine-exposed offspring. Therefore, we attempt to investigate the possible effect of prenatal morphine exposure on the vulnerability to hyperalgesia and the possible therapeutic effect of DM in the present study.MethodsFifty μl of carrageenan (20 mg/ml) was injected subcutaneously into the plantar surface of the right hind paw in p18 rats to induce hyperalgesia. Mean paw withdrawal latency was measured in the plantar test to index the severity of hyperalgesia. Using Western blotting and RT-PCR, the quantitative analyses of NMDA receptor NR1 and NR2B subunits were performed in spinal cords from different groups of animals.ResultsIn the carrageenan-induced hyperalgesia model, rat offspring passively exposed to morphine developed a severe hyperalgesia on postnatal day 18 (p18), which also had a more rapid time course than those in the controls. Co-administration of DM with morphine in the dams prevented this adverse effect of morphine in the offspring rats. Western blot and RT-PCR analysis showed that the levels of protein and mRNA of NMDA receptor NR1 and NR2B subunits were significantly higher in the lumbar spinal cords of rats (p14) exposed to prenatal morphine; the co-administration of DM could reverse the effect of morphine on NR1 and attenuate the effect on NR2B.ConclusionsThus, DM may have a great potential in the prevention of higher vulnerability to inflammatory thermal hyperalgesia in the offspring of morphine-addicted mothers.

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Coadministration of dextromethorphan during pregnancy and throughout lactation prevents morphine-induced hyperprolactinemia in female rats

Cited by 7 publications

References 52 publications

Attenuation by dextromethorphan on the higher liability to morphine-induced reward, caused by prenatal exposure of morphine in rat offspring

Attenuation by dextromethorphan on the higher liability to morphine-induced reward, caused by prenatal exposure of morphine in rat offspring

Beneficial effects of co-treatment with dextromethorphan on prenatally methadone-exposed offspring

Dextromethorphan attenuated the higher vulnerability to inflammatory thermal hyperalgesia caused by prenatal morphine exposure in rat offspring

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