Effect of a selective GABAB receptor agonist baclofen on the μ-opioid receptor agonist-induced antinociceptive, emetic and rewarding effects

Suzuki, Tsutomu; Nurrochmad, Arief; Masahiko, Ozaki; Khotib, Junaidi; Nakamura, Atsushi; Imai, Shoichi; Shibasaki, Manabu; Yajima, Yoshinori; Narita, Minoru

doi:10.1016/j.neuropharm.2005.06.009

Cited by 35 publications

(16 citation statements)

References 32 publications

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“…The dose of BAC (2 mg/kg) was selected based on our previous reports (Diaz et al, 2001(Diaz et al, , 2003(Diaz et al, , 2004, and this dose did not have intrinsic effect in nondependent animals. In agreement, a similar dose of BAC was reported by other authors (Fadda et al, 2003;Suzuki et al, 2005;Zarrindast and Mousa-Ahmadi, 1999). In the present study, BAC (2 mg/kg, i.p.)…”

Section: Discussionsupporting

confidence: 92%

Morphine withdrawal syndrome and its prevention with baclofen: Autoradiographic study of μ‐opioid receptors in prepubertal male and female mice

Diaz

Barros

Antonelli

et al. 2006

Synapse

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Although the expression of the morphine (MOR) withdrawal syndrome is more marked in male mice than in females, we have demonstrated that the GABAB agonist baclofen (BAC) is able to attenuate MOR withdrawal signs in either sex. In order to extend these previous observations, the aim of the present study was to evaluate the mu-opioid receptor labeling in various brain areas in mice of either sex, during MOR withdrawal and its prevention with BAC. Prepubertal Swiss-Webster mice were rendered dependent by intraperitonial (i.p.) injection of MOR (2 mg/kg) twice daily for 9 days. On the 10th day, dependent animals received naloxone (NAL; 6 mg/kg, i.p.) 60 min after MOR, and another pool of dependent mice received BAC (2 mg/kg, i.p.) previous to NAL. Thirty minutes after NAL, mice were sacrificed and autoradiography with [3H]-[D-Ala2, N-Me-Phe4, -glycol5] enkephalin (DAMGO) was carried out on mice brains at five different anatomical levels. Autoradiographic mapping showed a significant increase of mu-opioid receptor labeling during MOR withdrawal in nucleus accumbens core (NAcC), caudate putamen (CPu), mediodorsal thalamic nucleus (MDTh), basolateral and basomedial amygdala, and ventral tegmental area vs. respective control groups in male mice. In contrast, opiate receptor labeling was not significantly modified in any of the brain areas studied in withdrawn females. BAC reestablished mu-opioid receptor binding sites during MOR withdrawal only in NAcC of males, and a similar tendency was observed in CPu and MDTh, even when it was not statistically significant. The sexual dimorphism observed in the present study confirms previous reports indicating a greater sensitivity of males in response to MOR pharmacological properties. The present results suggest that the effect of BAC in preventing the expression of MOR withdrawal signs could be related with the ability of BAC to reestablish the mu-opioid receptor labeling in certain brain areas.

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Section: Discussionsupporting

confidence: 92%

Morphine withdrawal syndrome and its prevention with baclofen: Autoradiographic study of μ‐opioid receptors in prepubertal male and female mice

Diaz

Barros

Antonelli

et al. 2006

Synapse

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“…2003). Similarly, morphine (8 mg/kg sc)‐ and fentanyl (56 µg/kg sc)‐induced CPP was blocked by baclofen (1.5 and 3 mg/kg sc) (Suzuki et al . 2005).…”

Section: Studies Using Systemic Drug Treatmentsmentioning

confidence: 98%

“…Fentanyl (56 µg/kg sc) (Suzuki et al . 2005) and oxycodone (3 mg/kg sc) (Olmstead & Burns 2005) produced CPP.…”

Section: Studies Using Systemic Drug Treatmentsmentioning

confidence: 99%

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

2007

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Conditioned place preference (CPP) continues to be one of the most popular models to study the motivational effects of drugs and non-drug treatments in experimental animals. This is obvious from a steady year-to-year increase in the number of publications reporting the use this model. Since the compilation of the preceding review in 1998, more than 1000 new studies using place conditioning have been published, and the aim of the present review is to provide an overview of these recent publications. There are a number of trends and developments that are obvious in the literature of the last decade. First, as more and more knockout and transgenic animals become available, place conditioning is increasingly used to assess the motivational effects of drugs or non-drug rewards in genetically modified animals. Second, there is a still small but growing literature on the use of place conditioning to study the motivational aspects of pain, a field of pre-clinical research that has so far received little attention, because of the lack of appropriate animal models. Third, place conditioning continues to be widely used to study tolerance and sensitization to the rewarding effects of drugs induced by pre-treatment regimens. Fourth, extinction/reinstatement procedures in place conditioning are becoming increasingly popular. This interesting approach is thought to model certain aspects of relapse to addictive behavior and has previously almost exclusively been studied in drug self-administration paradigms. It has now also become established in the place conditioning literature and provides an additional and technically easy approach to this important phenomenon. The enormous number of studies to be covered in this review prevented in-depth discussion of many methodological, pharmacological or neurobiological aspects; to a large extent, the presentation of data had to be limited to a short and condensed summary of the most relevant findings.

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“…Another drug, baclofen, exerts its effects through GABA B receptor stimulation. In ferrets with induced emetic episodes, baclofen reduced the emetic response to morphine in a dose-dependent manner [82]. In addition, baclofen has been reported to reduce emesis in neurologically impaired children with gastroesophageal reflux disease [83].…”

Section: Conclusion and Future Perspectivementioning

confidence: 99%

Pharmacogenetics of Chemotherapy-Induced Nausea and Vomiting

Sugino

Janicki

2015

Pharmacogenomics

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Chemotherapy-induced nausea and vomiting (CINV) is associated with distressing adverse effects observed in patients during cytotoxic chemotherapy. One of the potential factors explaining suboptimal response to currently used antiemetics is variability in genes encoding enzymes and proteins that play a role in the action of antiemetic drugs. Pharmacogenomics studies of CINV are sparse and focus mainly on polymorphisms associated with serotonin receptor, drug metabolism and drug transport. Currently, the role of pharmacogenetics in mechanisms of CINV has not been fully unraveled, and it is premature to implement results of pharmacogenetic association studies of antiemetic drugs in clinical practice. More uniform studies, with genetic profiles and biomarkers relevant for the proposed target and transporter mechanisms, are needed.

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Effect of a selective GABAB receptor agonist baclofen on the μ-opioid receptor agonist-induced antinociceptive, emetic and rewarding effects

Cited by 35 publications

References 32 publications

Morphine withdrawal syndrome and its prevention with baclofen: Autoradiographic study of μ‐opioid receptors in prepubertal male and female mice

Morphine withdrawal syndrome and its prevention with baclofen: Autoradiographic study of μ‐opioid receptors in prepubertal male and female mice

REVIEW ON CPP: Measuring reward with the conditioned place preference (CPP) paradigm: update of the last decade

Pharmacogenetics of Chemotherapy-Induced Nausea and Vomiting

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