Assessment of SNC 80 and Naltrindole Within a Conditioned Taste Aversion Design

Hutchinson, A. C. W.; Simpson, Gregory R; Randall, Jovita F; Zhang, Xiaoyan; Calderon, Silvia N.; Rice, Kenner C.; Riley, Anthony L.

doi:10.1016/s0091-3057(00)00278-1

Cited by 14 publications

(6 citation statements)

References 81 publications

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“…, 1998). To maintain specificity, we used a relatively low concentration of naltrindole (1 mg/kg) (Hutchinson et al. , 2000), and we confirmed the ability of this systemic treatment to block DOR by testing SNC80‐induced responses in brains of naltrindole‐treated animals ex vivo .…”

Section: Resultsmentioning

confidence: 99%

Alterations of CXCR4 function in μ‐opioid receptor‐deficient glia

Burbassi

Sengupta

Meucci

2010

Eur J of Neuroscience

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The chemokine receptor CXCR4 and the μ-opioid receptor (MOR) are G-protein-coupled receptors (GPCRs) essential to normal function of the nervous and immune systems. Several studies suggest that MOR is a key regulator of CXCR4 in the brain; however, the molecular basis of the opioid/chemokine interaction are not fully understood and may involve different mechanisms in neuronal and glial cells. Our previous studies demonstrated that MOR stimulation specifically up-regulates the protein ferritin heavy chain (FHC) -an inhibitor of CXCR4 -in neurons and suggested additional mechanisms could be operative in glial cells. In this study, we investigated CXCR4 function in brains and astroglia cultures deprived of MOR. Reduced coupling of CXCR4 to G proteins was found in brain slices and tissue homogenates of MOR−/− mice compared to wild type (WT) controls. CXCR4-induced signaling was also reduced in glial cultures from MOR−/− mice, as shown by analysis of CXCR4 downstream targets (Akt and ERK1/2). Pharmacological studies with δ-opioid receptor (DOR)-specific ligands suggested that DOR-CXCR4 interactions are implicated in the inhibition of CXCR4 in MOR-deficient cells both in vitro and in vivo. Moreover, increased CXCR4/DOR co-immunoprecipitation was found in brain tissue and cultured glia from MOR−/− mice. Importantly, CXCR4 function was restored by pretreatment with a DOR antagonist. Overall, these findings indicate that DOR play a crucial role in the regulation of CXCR4 in glia, likely via silent receptor heterodimers. The data also suggest that the opiate system interferes with normal CXCR4 function in different ways and depending on receptor subtypes.

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Section: Resultsmentioning

confidence: 99%

Alterations of CXCR4 function in μ‐opioid receptor‐deficient glia

Burbassi

Sengupta

Meucci

2010

Eur J of Neuroscience

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“…Indeed, stimulation of -opioid receptors through endogenous dynorphins in response to other dysphoric-aversive stimuli has been reported (Staley et al, 1997;Hutchinson et al, 2000). Additional studies will be performed to determine whether the motivational responses of other aversive stimulus are also modified in prodynorphin knockout mice.…”

Section: Discussionmentioning

confidence: 96%

Absence of Δ-9-Tetrahydrocannabinol Dysphoric Effects in Dynorphin-Deficient Mice

et al. 2001

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The involvement of dynorphin on ⌬-9-tetrahydrocannabinol (THC) and morphine responses has been investigated by using mice with a targeted inactivation of the prodynorphin (Pdyn) gene. Dynorphin-deficient mice show specific changes in the behavioral effects of THC, including a reduction of spinal THC analgesia and the absence of THC-induced conditioned place aversion. In contrast, acute and chronic opioid effects were normal. The lack of negative motivational effects of THC in the absence of dynorphin demonstrates that this endogenous opioid peptide mediates the dysphoric effects of marijuana.Key words: cannabinoid; opioid; mice; mutation; withdrawal; addiction; place aversion Pharmacological and genetic evidence suggest important functional interactions between the endogenous brain cannabinoid and opioid systems (Hine et al

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“…The δ‐agonist, SNC80, abolished NTG‐evoked place aversion. SNC80 alone has been previously reported to produce conditioned place preference (Longoni et al ., ); or under other circumstances, conditioned taste aversion (Hutchinson et al ., ). In our study, however, SNC80 (vehicle‐SNC80 group, Figure ) produced neither preference nor aversion, most likely due to differences in experimental design.…”

Section: Discussionmentioning

confidence: 97%

δ‐Opioid receptor agonists inhibit migraine‐related hyperalgesia, aversive state and cortical spreading depression in mice

Pradhan

Smith

Zyuzin³

et al. 2014

British J Pharmacology

132

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BACKGROUND AND PURPOSEMigraine is an extraordinarily common brain disorder for which treatment options continue to be limited. Agonists that activate the δ-opioid receptor may be promising for the treatment of migraine as they are highly effective for the treatment of chronic rather than acute pain, do not induce hyperalgesia, have low abuse potential and have anxiolytic and antidepressant properties. The aim of this study was to investigate the therapeutic potential of δ-opioid receptor agonists for migraine by characterizing their effects in mouse migraine models. EXPERIMENTAL APPROACHMechanical hypersensitivity was assessed in mice treated with acute and chronic doses of nitroglycerin (NTG), a known human migraine trigger. Conditioned place aversion to NTG was also measured as a model of migraine-associated negative affect. In addition, we assessed evoked cortical spreading depression (CSD), an established model of migraine aura, in a thinned skull preparation. KEY RESULTSNTG evoked acute and chronic mechanical and thermal hyperalgesia in mice, as well as conditioned place aversion. Three different δ-opioid receptor agonists, SNC80, ARM390 and JNJ20788560, significantly reduced NTG-evoked hyperalgesia. SNC80 also abolished NTG-induced conditioned place aversion, suggesting that δ-opioid receptor activation may also alleviate the negative emotional state associated with migraine. We also found that SNC80 significantly attenuated CSD, a model that is considered predictive of migraine preventive therapies. CONCLUSIONS AND IMPLICATIONSThese data show that δ-opioid receptor agonists modulate multiple basic mechanisms associated with migraine, indicating that δ-opioid receptors are a promising therapeutic target for this disorder. Abbreviations

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Assessment of SNC 80 and Naltrindole Within a Conditioned Taste Aversion Design

Cited by 14 publications

References 81 publications

Alterations of CXCR4 function in μ‐opioid receptor‐deficient glia

Alterations of CXCR4 function in μ‐opioid receptor‐deficient glia

Absence of Δ-9-Tetrahydrocannabinol Dysphoric Effects in Dynorphin-Deficient Mice

δ‐Opioid receptor agonists inhibit migraine‐related hyperalgesia, aversive state and cortical spreading depression in mice

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