Efficacy of Chronic Morphine in a Rat Model of Cancer-Induced Bone Pain: Behavior and in Dorsal Horn Pathophysiology

Urch, Catherine; Donovan-Rodríguez, Tansy; Gordon-Williams, Richard; Bee, Lucy; Dickenson, Anthony H.

doi:10.1016/j.jpain.2005.08.005

Cited by 42 publications

(33 citation statements)

References 25 publications

(35 reference statements)

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“…We have previously reported on the effects of systemic morphine on the responses of these neurones (Urch et al, 2005). A dose of 3 mg/kg produced effects that were of a similar magnitude but were less pronounced than tapentadol on responses evoked by the lower mechanical forces.…”

Section: Tapentadol Analgesia In Cancer Painmentioning

confidence: 90%

Spinal neuronal correlates of tapentadol analgesia in cancer pain: A back‐translational approach

Falk

Patel

Heegaard

et al. 2014

European Journal of Pain

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Background: Pain is a common and highly debilitating complication for cancer patients significantly compromising their quality of life. Cancer-induced bone pain involves a complex interplay of multiple mechanisms including both inflammatory and neuropathic processes and also some unique changes. Strong opioids are a mainstay of treatments but side effects are problematic and can compromise optimal pain control. Tapentadol is a novel dual-action drug, both stimulating inhibitory μ-opioid receptors (MOR) and mediating noradrenaline reuptake inhibition (NRI) leading to activation of the inhibitory α-2 adrenoceptor. It has been demonstrated to treat effectively both acute and chronic pain. We here demonstrate the efficacy in a model of cancer-induced bone pain. Methods: MRMT-1 mammary carcinoma cells were inoculated into the tibia of 6-week-old rats and 2 weeks after, the neuronal responses to a wide range of peripheral stimulation were evaluated. The recordings were made from wide-dynamic range neurons in lamina V of the dorsal horn before and after administration of tapentadol as well as antagonists of the two mechanisms, naloxone or atipamezole. Results: We found marked inhibitions of the neuronal activity with efficacy against mechanical, thermal and electrically evoked activity following tapentadol administration. In addition, the effects of the drug were fully reversible by naloxone and partly by atipamezole, supporting the idea of MOR-NRI dual actions. Conclusions: These findings add to the mechanistic understanding of cancer-induced bone pain and support the sparse clinical data indicating a possible use of the drug as a therapeutic alternative for cancer patients with metastatic pain complication.

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Section: Tapentadol Analgesia In Cancer Painmentioning

confidence: 90%

Spinal neuronal correlates of tapentadol analgesia in cancer pain: A back‐translational approach

Falk

Patel

Heegaard

et al. 2014

European Journal of Pain

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“…Data regarding opioid tolerance in animal models of inflammation, injury and disease are few and inconsistent. Some behavioural studies suggest that tolerance to the anti-nociceptive effects (withdrawal effects) of opioids develop more slowly in inflammatory (Vaccarino et al., 1993; Zollner et al., 2008), cancer (Urch et al., 2005) and neuropathic models (Iwai et al., 2012) when compared to sham controls. Other studies demonstrate enhanced development of analgesic tolerance, particularly in neuropathic models (Raghavendra et al., 2002).…”

Section: Opioid Tolerance and Drug-induced Hyperalgesiamentioning

confidence: 99%

Imaging opioid analgesia in the human brain and its potential relevance for understanding opioid use in chronic pain

2014

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Opioids play an important role for the management of acute pain and in palliative care. The role of long-term opioid therapy in chronic non-malignant pain remains unclear and is the focus of much clinical research. There are concerns regarding analgesic tolerance, paradoxical pain and issues with dependence that can occur with chronic opioid use in the susceptible patient. In this review, we discuss how far human neuroimaging research has come in providing a mechanistic understanding of pain relief provided by opioids, and suggest avenues for further studies that are relevant to the management of chronic pain with opioids.This article is part of the Special Issue Section entitled ‘Neuroimaging in Neuropharmacology’.

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“…Sustained morphine administration reverses cancer pain behavior in a rat cancer model produced by inoculating MRMT-1 cells. Dorsal horn plasticity, however, remains unchanged (Urch and others 2005). …”

Section: Preclinical Studiesmentioning

confidence: 99%

The Neurobiology of Cancer Pain

Schmidt

2014

Neuroscientist

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The global burden of cancer pain is enormous and opioids, despite their side effects, remain the primary therapeutic approach. The cause of cancer pain is unknown. Mechanisms driving cancer pain differ from those mechanisms responsible for inflammatory and neuropathic pain. The prevailing hypothesis put forward to explain cancer pain posits that cancers generate and secrete mediators which sensitize and activate primary afferent nociceptors in the cancer microenvironment. Moreover, cancers induce neurochemical reorganization of the spinal cord, which contributes to spontaneous activity and enhanced responsiveness. The purpose of this review, which covers clinical and preclinical studies, is to highlight those peripheral and central mechanisms responsible for cancer pain. The challenges facing neuroscientists and clinicians studying and ultimately treating cancer pain are discussed.

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Efficacy of Chronic Morphine in a Rat Model of Cancer-Induced Bone Pain: Behavior and in Dorsal Horn Pathophysiology

Cited by 42 publications

References 25 publications

Spinal neuronal correlates of tapentadol analgesia in cancer pain: A back‐translational approach

Spinal neuronal correlates of tapentadol analgesia in cancer pain: A back‐translational approach

Imaging opioid analgesia in the human brain and its potential relevance for understanding opioid use in chronic pain

The Neurobiology of Cancer Pain

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