Sex differences in hyperalgesia during morphine infusion: Effect of gonadectomy and estrogen treatment

Juni, Aaron; Klein, Gad; Kowalczyk, William J.; Ragnauth, Andre; Kest, Benjamin

doi:10.1016/j.neuropharm.2008.04.004

Cited by 42 publications

(64 citation statements)

References 33 publications

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“…Thus far, a host of animal studies have found that OIH is reversible by the NMDA receptor antagonists MK-801 [31,42,[160][161][162][163][164][165], ketamine, or traxoprodil [93]. Human studies have found similar results by adding adjuvant ketamine [46,54,88,166], as well as gabapentinoids such as pregabalin [49,55] or gabapentin [23], or the cyclooxygenase-2 inhibitor parecoxib [48,167], as reviewed in the subsequent sections.…”

Section: Prospective Treatments For Oihmentioning

confidence: 97%

Targeting Opioid-Induced Hyperalgesia in Clinical Treatment: Neurobiological Considerations

et al. 2015

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Opioid analgesics have become a cornerstone in the treatment of moderate to severe pain, resulting in a steady rise of opioid prescriptions. Subsequently, there has been a striking increase in the number of opioid-dependent individuals, opioid-related overdoses, and fatalities. Clinical use of opioids is further complicated by an increasingly deleterious profile of side effects beyond addiction, including tolerance and opioid-induced hyperalgesia (OIH), where OIH is defined as an increased sensitivity to already painful stimuli. This paradoxical state of increased nociception results from acute and long-term exposure to opioids, and appears to develop in a substantial subset of patients using opioids. Recently, there has been considerable interest in developing an efficacious treatment regimen for acute and chronic pain. However, there are currently no well-established treatments for OIH. Several substrates have emerged as potential modulators of OIH, including the N-methyl-D-aspartate and γ-aminobutyric acid receptors, and most notably, the innate neuroimmune system. This review summarizes the neurobiology of OIH in the context of clinical treatment; specifically, we review evidence for several pathways that show promise for the treatment of pain going forward, as prospective adjuvants to opioid analgesics. Overall, we suggest that this paradoxical state be considered an additional target of clinical treatment for chronic pain.

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Section: Prospective Treatments For Oihmentioning

confidence: 97%

Targeting Opioid-Induced Hyperalgesia in Clinical Treatment: Neurobiological Considerations

et al. 2015

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“…Nature Reviews | Neuroscience qualitative sex differences in the midbrain, spinal cord and the primary afferent -are currently more comprehensively documented than the others. Multiple laboratories have observed that the midbrain-brain stem neural circuit subserving stress-induced analgesia, κ-opioid (and possibly μ-opioid) analgesia, morphine tolerance and morphine hyperalgesia in mice contains NMDAtype glutamate receptors (NMDARs) in males 49,56,57,[88][89][90] but not females; in many cases, females seem to use melanocortin 1 receptors (MC1Rs) instead 39,54,91 . In these studies, pharmacological antagonism with non-competitive NMDAR antagonists (for example, MK-801) blocks the phenomena in male but not female mice at any dose.…”

Section: Nature Reviews | Neurosciencementioning

confidence: 99%

Sex differences in pain and pain inhibition: multiple explanations of a controversial phenomenon

2012

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| A clear majority of patients with chronic pain are women; however, it has been surprisingly difficult to determine whether this sex bias corresponds to actual sex differences in pain sensitivity. A survey of the currently available epidemiological and laboratory data indicates that the evidence for clinical and experimental sex differences in pain is overwhelming. Various explanations for this phenomenon have been given, ranging from experiential and sociocultural differences in pain experience between men and women to hormonally and genetically driven sex differences in brain neurochemistry. PERSPECTIVES NATURE REVIEWS | NEUROSCIENCE VOLUME 13 | DECEMBER 2012 | 859

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“…Despite this selection bias, the emerging view was to consider males as better responders to opiate analgesics 49,50 , less prone to develop opioid-induced hyperalgesia 51,52 and more tolerant to morphine analgesia 53 than their female counterparts (review . For example, global analysis of fifty clinical trials indicated no significant differences in analgesic properties between genders whereas meta-analyses performed on patients-controlled subjects pointed to a significantly greater opioid efficacy in women 57 .The latter observation, which markedly contrasts with what has been found in rodents, again raises several questions regarding the origin for such divergences 16,48,55,57 .…”

Section: Sex Differences In Pain and Analgesiamentioning

confidence: 99%

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities

Elhabazi¹,

Ayachi²,

Ilien³

et al. 2014

JoVE

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Opioid-induced hyperalgesia and tolerance severely impact the clinical efficacy of opiates as pain relievers in animals and humans. The molecular mechanisms underlying both phenomena are not well understood and their elucidation should benefit from the study of animal models and from the design of appropriate experimental protocols.We describe here a methodological approach for inducing, recording and quantifying morphine-induced hyperalgesia as well as for evidencing analgesic tolerance, using the tail-immersion and tail pressure tests in wild-type mice. As shown in the video, the protocol is divided into five sequential steps. Handling and habituation phases allow a safe determination of the basal nociceptive response of the animals. Chronic morphine administration induces significant hyperalgesia as shown by an increase in both thermal and mechanical sensitivity, whereas the comparison of analgesia time-courses after acute or repeated morphine treatment clearly indicates the development of tolerance manifested by a decline in analgesic response amplitude. This protocol may be similarly adapted to genetically modified mice in order to evaluate the role of individual genes in the modulation of nociception and morphine analgesia. It also provides a model system to investigate the effectiveness of potential therapeutic agents to improve opiate analgesic efficacy.

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Sex differences in hyperalgesia during morphine infusion: Effect of gonadectomy and estrogen treatment

Cited by 42 publications

References 33 publications

Targeting Opioid-Induced Hyperalgesia in Clinical Treatment: Neurobiological Considerations

Targeting Opioid-Induced Hyperalgesia in Clinical Treatment: Neurobiological Considerations

Sex differences in pain and pain inhibition: multiple explanations of a controversial phenomenon

Assessment of Morphine-induced Hyperalgesia and Analgesic Tolerance in Mice Using Thermal and Mechanical Nociceptive Modalities

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