The puerperium alters spinal cord plasticity following peripheral nerve injury

Gutiérrez, Sílvia; Hayashida, Ken–ichiro; Eisenach, James C.

doi:10.1016/j.neuroscience.2012.10.039

Cited by 24 publications

(16 citation statements)

References 31 publications

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“…Estrogen derivatives modulate CNS processing of chronic pain (135, 136), and female mice have slower nerve regeneration at the injury site and more reactive gliosis in the SDH than male mice. Furthermore, the administration of sex steroids in studies of pain responses can influence levels of spinal dynorphin (135, 137). Women respond differently to opioid treatments for chronic pain conditions, experiencing higher rates of opioid-induced hyperalgesia (OIH) than men (134).…”

Section: Human Chronic Pain and Dynorphinmentioning

confidence: 99%

The Emerging Role of Spinal Dynorphin in Chronic Pain: A Therapeutic Perspective

Podvin

Yaksh²,

Hook

2016

Annu. Rev. Pharmacol. Toxicol.

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Notable findings point to the significance of the dynorphin peptide neurotransmitter in chronic pain. Spinal dynorphin neuropeptide levels are elevated during development of chronic pain. Importantly, knockout of the dynorphin gene prevents development of chronic pain in mice, but acute nociception is unaffected. Intrathecal (IT) administration of opioid and non-opioid dynorphin peptides initiate allodynia through a non-opioid receptor mechanism; furthermore, anti-dynorphin antibodies administered by the IT route attenuate chronic pain. Thus, this review presents the compelling evidence in the field supporting the role of dynorphin in facilitating the development of a persistent pain state. These observations raise the question of the control mechanisms responsible for the upregulation of spinal dynorphin leading to chronic pain development. Also, spinal dynorphin regulation of downstream signaling molecules may be implicated in hyperpathic states. Therapeutic strategies to reduce spinal dynorphin may provide a non-addictive approach to improve the devastating condition of chronic pain that occurs in numerous human diseases.

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Section: Human Chronic Pain and Dynorphinmentioning

confidence: 99%

The Emerging Role of Spinal Dynorphin in Chronic Pain: A Therapeutic Perspective

Podvin

Yaksh²,

Hook

2016

Annu. Rev. Pharmacol. Toxicol.

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“…For both male and female mice, nerve injury induces the same degree of astrocyte activation, as measured by GFAP expression in the spinal cord, and inhibitors of astroglial signaling have been found to reduce inflammatory and neuropathic pain (Chen et al, 2018). However, a lack of astrocyte activation in female rats after nerve injury has also been reported (Gutierrez et al, 2013). Currently, it is unclear whether other immune cells or glial cells, including macrophages, have sexdimorphic roles in chronic pain.…”

Section: Introductionmentioning

confidence: 99%

Macrophage Toll-like Receptor 9 Contributes to Chemotherapy-Induced Neuropathic Pain in Male Mice

Luo¹,

Huh

Bang³

et al. 2019

J. Neurosci.

111

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Chemotherapy-induced peripheral neuropathy (CIPN) remains a pressing clinical problem; however, our understanding of sexual dimorphism in CIPN remains unclear. Emerging studies indicate a sex-dimorphic role of Toll-like receptor 4 (TLR4) in driving neuropathic pain. In this study, we examined the role of TLR9 in CIPN induced by paclitaxel in WT and Tlr9 mutant mice of both sexes. Baseline pain sensitivity was not affected in either Tlr9 mutant male or female mice. Intraplantar and intrathecal injection of the TLR9 agonist ODN 1826 induced mechanical allodynia in both sexes of WT and Tlr4 KO mice but failed to do so in Tlr9 mutant mice. Moreover, Trpv1 KO or C-fiber blockade by resiniferatoxin failed to affect intraplantar ODN 1826-induced mechanical allodynia. Interestingly, the development of paclitaxel-evoked mechanical allodynia was attenuated by TLR9 antagonism or Tlr9 mutation only in male mice. Paclitaxel-induced CIPN caused macrophage infiltration to DRGs in both sexes, and this infiltration was not affected by Tlr9 mutation. Paclitaxel treatment also upregulated TNF and CXCL1 in macrophage cultures and DRG tissues in both sexes, but these changes were compromised by Tlr9 mutation in male animals. Intraplantar adoptive transfer of paclitaxel-activated macrophages evoked mechanical allodynia in both sexes, which was compromised by Tlr9 mutation or by treatment with TLR9 inhibitor only in male animals. Finally, TLR9 antagonism reduced paclitaxel-induced mechanical allodynia in female nude mice (T-cell and B-cell deficient). Together, these findings reveal sex-dimorphic macrophage TLR9 signaling in chemotherapy-induced neuropathic pain.

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“…Importantly, partial reversal of peripheral nerve injury pain does not happen in lactating rodent females in the absence of pups (Gutierrez et al, 2013b ). Since labor and breastfeeding promote elevation of OXT in blood as well as cerebrospinal fluid (Gutierrez et al, 2013b ) and since PVN afferents project to the spinal cord (Reiter et al, 1994 ; Eliava et al, 2016 ), it is hypothesized that exogenous OXT could be used as an anti-hyperalgesia drug in a variety of pain conditions (Breton et al, 2008 ; Gutierrez et al, 2013a , b ; Boll et al, 2017 ). Indeed, direct administration of OXT into the spinal cord produced analgesia in a patient with intractable cancer pain (Madrazo et al, 1987 ).…”

Section: Oxytocinmentioning

confidence: 99%

Pituitary Hormones and Orofacial Pain

Dussor

Boyd

Akopian

2018

Front. Integr. Neurosci.

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Clinical and basic research on regulation of pituitary hormones, extra-pituitary release of these hormones, distribution of their receptors and cell signaling pathways recruited upon receptor binding suggests that pituitary hormones can regulate mechanisms of nociceptive transmission in multiple orofacial pain conditions. Moreover, many pituitary hormones either regulate glands that produce gonadal hormones (GnH) or are regulated by GnH. This implies that pituitary hormones may be involved in sex-dependent mechanisms of orofacial pain and could help explain why certain orofacial pain conditions are more prevalent in women than men. Overall, regulation of nociception by pituitary hormones is a relatively new and emerging area of pain research. The aims of this review article are to: (1) present an overview of clinical conditions leading to orofacial pain that are associated with alterations of serum pituitary hormone levels; (2) discuss proposed mechanisms of how pituitary hormones could regulate nociceptive transmission; and (3) outline how pituitary hormones could regulate nociception in a sex-specific fashion. Pituitary hormones are routinely used for hormonal replacement therapy, while both receptor antagonists and agonists are used to manage certain pathological conditions related to hormonal imbalance. Administration of these hormones may also have a place in the treatment of pain, including orofacial pain. Hence, understanding the involvement of pituitary hormones in orofacial pain, especially sex-dependent aspects of such pain, is essential to both optimize current therapies as well as provide novel and sex-specific pharmacology for a diversity of associated conditions.

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The puerperium alters spinal cord plasticity following peripheral nerve injury

Cited by 24 publications

References 31 publications

The Emerging Role of Spinal Dynorphin in Chronic Pain: A Therapeutic Perspective

The Emerging Role of Spinal Dynorphin in Chronic Pain: A Therapeutic Perspective

Macrophage Toll-like Receptor 9 Contributes to Chemotherapy-Induced Neuropathic Pain in Male Mice

Pituitary Hormones and Orofacial Pain

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