Plasma corticosterone levels in mouse models of pain

Benedetti, M.; Merino, Rubén; Kusuda, Ricardo; Ravanelli, Maria Ida Bonini; Cadetti, F.; Santos, Paula; Zanon, Sonia; Lucas, Guilherme

doi:10.1002/j.1532-2149.2011.00066.x

Cited by 51 publications

(40 citation statements)

References 77 publications

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“…The serum corticosterone concentration in OB-Sham group was significantly higher than that in NOB-Sham group ( p = 0.004) suggesting an increased activity of HPA axis induced by OB, which has been reported in previous studies (Marcilhac et al, 1999; Cryan and Mombereau, 2004). No difference was found in the serum corticosterone concentrations between NOB-SNL group and NOB-Sham group ( p = 0.516), which is consistent with previous observations (Ulrich-Lai et al, 2006; Alexander et al, 2009; Benedetti et al, 2012). Interestingly, corticosterone level in OB-SNL group was lower than that in OB-Sham group ( p < 0.001) and NOB-SNL group ( p = 0.048), indicating a decreased activity of HPA axis, which may due to the exhausted state of HPA axis in OB rats following SNL surgery.…”

Section: Resultssupporting

confidence: 92%

Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain

Xiao

Sun

Luo

2017

Front. Cell. Neurosci.

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Although depression-induced altered pain perception has been described in several laboratory and clinical studies, its neurobiological mechanism in the central nervous system (CNS), particularly in the spinal dorsal horn, remains unclear. Therefore, in this study, we aimed to clarify whether nociceptive sensitivity of neuropathic pain is altered in the olfactory bulbectomy (OB) model of depression and whether glucocorticoid receptor (GR), which is involved in the etio-pathologic mechanisms of both major depression and neuropathic pain, contributes to these processes in the spinal dorsal horn of male Sprague-Dawley rats. The results showed that mechanical allodynia and thermal hyperalgesia induced by spinal nerve ligation (SNL) were attenuated in OB-SNL rats with decreased spinal GR expression and nuclear translocation, whereas non-olfactory bulbectomy (NOB)-SNL rats showed increased spinal GR nuclear translocation. In addition, decreased GR nuclear translocation with normal mechanical nociception and hypoalgesia of thermal nociception were observed in OB-Sham rats. Intrathecal injection (i.t.) of GR agonist dexamethasone (Dex; 4 μg/rat/day for 1 week) eliminated the attenuating effect of depression on nociceptive hypersensitivity in OB-SNL rats and aggravated neuropathic pain in NOB-SNL rats, which was associated with the up-regulation of brain-derived neurotrophic factor (BDNF), TrkB and NR2B expression in the spinal dorsal horn. The present study shows that depression attenuates the mechanical allodynia and thermal hyperalgesia of neuropathic pain and suggests that altered spinal GR-BDNF-TrkB signaling may be one of the reasons for depression-induced hypoalgesia.

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Section: Resultssupporting

confidence: 92%

Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain

Xiao

Sun

Luo

2017

Front. Cell. Neurosci.

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“…However, it is noteworthy that corticosterone levels in the untested obese HFD mice were significantly elevated 18–20 hours after capsaicin treatment. Others have observed normalization of capsaicin-evoked corticosterone by 3 hours in C57BL/6J mice 1 , suggesting that obesity prolongs HPA axis activation evoked by capsaicin. Prolonged HPA axis activation in response to pain could have implications for pain modulation, especially in disorders of recurrent or chronic pain.…”

Section: Discussionmentioning

confidence: 95%

Abnormal trigeminal sensory processing in obese mice

Rossi

Broadhurst

Luu

et al. 2016

Pain

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“…Some researchers reported higher levels of corticosterone in human patients with chronic back pain (Vachon-Presseau et al, 2013), while others not (Muhtz et al, 2013). In mice, persistent increase of corticosterone has been found in inflammatory pain models (Zheng et al, 2017), while an acute increase or no change of corticosterone was reported in neuropathic pain models (Yalcin et al, 2011; Benedetti et al, 2012). To minimize the effects of stress hormones on the results, we adopted neuropathic pain model in the present study.…”

Section: Discussionmentioning

confidence: 99%

Anxiety Specific Response and Contribution of Active Hippocampal Neural Stem Cells to Chronic Pain Through Wnt/β-Catenin Signaling in Mice

Zhao

Zhang

Wang

et al. 2018

Front. Mol. Neurosci.

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Chronic pain usually results in persistent anxiety, which worsens the life quality of patients and complicates the treatment of pain. Hippocampus is one of the few brain regions in many mammalians species which harbors adult neural stem cells (NSCs), and plays a key role in the development and maintenance of chronic anxiety. Recent studies have suggested a potential involvement of hippocampal neurogenesis in modulating chronic pain. Whether and how hippocampal NSCs are involved in the pain-associated anxiety remains unclear. Here, we report that mice suffering persistent neuropathic pain showed a quick reduction of active NSCs in the ventral dentate gyrus (vDG), which was followed by the decrease of neurogenesis and appearance of anxiety. Wnt/β-catenin signaling, a key pathway in sustaining the active status of NSCs was suppressed in the vDG of mice suffering chronic pain. Depleting β-catenin by inducible Nestin-Cre significantly reduced the number of active NSCs and facilitated anxiety development, while expressing stabilized β-catenin amplified active NSCs and alleviated anxiety, indicating that Wnt activated NSCs is required for anxiety development under chronic pain. Treatment with Fluoxetine, the most widely used anxiolytic in clinic, significantly increased the proliferation of active NSCs and enhanced Wnt signaling. Interestingly, both β-catenin manipulation and Fluoxetine treatment had no significant effects on the pain thresholds. Therefore, our data demonstrated an anxiety-specific response and contribution of activated NSCs to chronic pain through Wnt/β-catenin signaling, which may be targeted for treating chronic pain- or other diseases-associated anxiety.

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Plasma corticosterone levels in mouse models of pain

Cited by 51 publications

References 77 publications

Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain

Impaired Spinal Glucocorticoid Receptor Signaling Contributes to the Attenuating Effect of Depression on Mechanical Allodynia and Thermal Hyperalgesia in Rats with Neuropathic Pain

Abnormal trigeminal sensory processing in obese mice

Anxiety Specific Response and Contribution of Active Hippocampal Neural Stem Cells to Chronic Pain Through Wnt/β-Catenin Signaling in Mice

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