Effects of capsazepine, a transient receptor potential vanilloid type 1 antagonist, on morphine-induced antinociception, tolerance, and dependence in mice

Nguyen, Thi-Lien; Nam, Y.-S.; Lee, S.-Y.; Kim, H.-C.; Jang, Choon‐Gon

doi:10.1093/bja/aeq212

Cited by 49 publications

(31 citation statements)

References 38 publications

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“…Moreover, upregulation of TRPV1 in the dorsal root ganglion, spinal cord, and sciatic nerve through mitogen-activated protein kinase pathways after chronic morphine treatment contributed to morphine tolerance in rats (Chen et al, 2008). Recently, we reported that blocking TRPV1 with a TRPV1 antagonist, capsazepine, attenuated morphine tolerance and withdrawal symptoms in mice (Nguyen et al, 2010). Taken together, these data imply that TRPV1 may be a molecular target in morphine reward.…”

Section: Introductionmentioning

confidence: 77%

Transient Receptor Potential Vanilloid Type 1 Channel May Modulate Opioid Reward

Nguyen

Kwon

Hong

et al. 2014

Neuropsychopharmacol

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Transient receptor potential vanilloid type 1 (TRPV1), a nonselective cation channel, is a well-known pain-related receptor. TRPV1 involvement in morphine-induced antinociception, tolerance, and withdrawal symptoms has been previously reported. Emerging evidence indicates that TRPV1 may be related to both the cellular and behavioral effects of addictive drugs. In the present study, we investigated the role of TRPV1 in morphine reward using the conditioned place preference (CPP) paradigm in mice. Repeated morphine treatments upregulated TRPV1 expression in the dorsal striatum (DSt). Treatment with a TRPV1 agonist potentiated morphine reward, and pretreatment with TRPV1 antagonists attenuated these effects. Microinjection of a selective TRPV1 antagonist into the DSt significantly inhibited morphine-CPP. In addition, treatment with a TRPV1 antagonist suppressed morphine-induced increases in m-opioid receptor binding, adenylyl cyclase 1 (AC1), p38 mitogen-activated protein kinase (p38 MAPK), and nuclear factor kappa B (NF-kB) expression in the DSt. Administering a p38 inhibitor not only prevented morphine-CPP, but also prevented morphine-induced NF-kB and TRPV1 activation in the DSt. Furthermore, injecting an NF-kB inhibitor significantly blocked morphine-CPP. Our findings suggest that TRPV1 in the DSt contribute to morphine reward via AC1, p38 MAPK, and NF-kB. Brain TRPV1 may serve as a novel therapeutic target to treat morphine-addictive disorders.

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Section: Introductionmentioning

confidence: 77%

Transient Receptor Potential Vanilloid Type 1 Channel May Modulate Opioid Reward

Nguyen

Kwon

Hong

et al. 2014

Neuropsychopharmacol

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“…23 In accordance with the results of previous studies, a recent report indicated blocking TRPV1 receptors with capsazepine (2.5 mg kg -1 ) inhibited morphine tolerance induced by five days of morphine treatment. 24 The results of these studies suggest that sustained opioid exposure also enhances TRPV1 receptor function in the periphery and plays an additional and essential role in sustained morphine induced thermal and tactile hypersensitivity.…”

Section: Introductionmentioning

confidence: 94%

“…Furthermore, our data first demonstrated that TRPV1 antagonists significantly reduced withdrawal symptoms in morphine-dependent mice. 24 …”

Section: Introductionmentioning

confidence: 99%

The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence

et al. 2015

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Initiated by the activation of various nociceptors, pain is a reaction to specific stimulus modalities. The μ-opioid receptor (MOR) agonists, including morphine, remain the most potent analgesics to treat patients with moderate to severe pain. However, the utility of MOR agonists is limited by the adverse effects associated with the use of these drugs, including analgesic tolerance and physical dependence. A strong connection has been suggested between the expression of the transient receptor potential vanilloid type 1 (TRPV1) ion channel and the development of inflammatory hyperalgesia. TRPV1 is important for thermal nociception induction, and is mainly expressed on sensory neurons. Recent reports suggest that opioid or TRPV1 receptor agonist exposure has contrasting consequences for anti-nociception, tolerance and dependence. Chronic morphine exposure modulates TRPV1 activation and induces the anti-nociception effects of morphine. The regulation of many downstream targets of TRPV1 plays a critical role in this process, including calcitonin gene-related peptide (CGRP) and substance P (SP). Additional factors also include capsaicin treatment blocking the anti-nociception effects of morphine in rats, as well as opioid modulation of TRPV1 responses through the cAMP-dependent PKA pathway and MAPK signaling pathways. Here, we review new insights concerning the mechanism underlying MOR-TRPV1 crosstalk and signaling pathways and discuss the potential mechanisms of morphine-induced anti-nociception, tolerance and dependence associated with the TRPV1 signaling pathway and highlight how understanding these mechanisms might help find therapeutic targets for the treatment of morphine induced antinociception, tolerance and dependence.

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“…Their therapeutic potential is being explored in inflammatory [5,6], cardiovascular [7,8], neurodegenerative [9,10], neoplasic diseases [11,12], as well as other disorders [13,14]. The presence of the 4-hydroxy-3-methoxy phenyl residue allows them to specifically interact with sensory neurons, and from this point of view, capsaicin has been used to treat peripheral painful conditions and neuropathies [10,15,16]. It was shown that curcumin regulates the classical and the alternative pathway of nervous system, being used in the treatment of Alzheimer, multiple sclerosis and dementia [9,10,17].…”

Section: Introductionmentioning

confidence: 99%

Guaicolic spices curcumin and capsaicin electrochemical oxidation behaviour at a glassy carbon electrode

Manaia

Diculescu

Gil

et al. 2012

Journal of Electroanalytical Chemistry

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Effects of capsazepine, a transient receptor potential vanilloid type 1 antagonist, on morphine-induced antinociception, tolerance, and dependence in mice

Abstract: Our results suggest that TRPV1 antagonists can be used adjunctively to morphine treatment because they strengthen morphine antinociception and prevent the development of tolerance, and also physical dependence, on morphine.

Cited by 49 publications

References 38 publications

Transient Receptor Potential Vanilloid Type 1 Channel May Modulate Opioid Reward

Transient Receptor Potential Vanilloid Type 1 Channel May Modulate Opioid Reward

The mechanism of μ-opioid receptor (MOR)-TRPV1 crosstalk in TRPV1 activation involves morphine anti-nociception, tolerance and dependence

Guaicolic spices curcumin and capsaicin electrochemical oxidation behaviour at a glassy carbon electrode

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