scholarly journals Reduction of Bone Cancer Pain by Activation of Spinal Cannabinoid Receptor 1 and Its Expression in the Superficial Dorsal Horn of the Spinal Cord in a Murine Model of Bone Cancer Pain

2009 ◽  
Vol 111 (1) ◽  
pp. 173-186 ◽  
Author(s):  
Shingo Furuse ◽  
Tomoyuki Kawamata ◽  
Jun Yamamoto ◽  
Yukitoshi Niiyama ◽  
Keiichi Omote ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Cancer Pain ◽  
Dorsal Horn ◽  
Cannabinoid Receptor ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Superficial Dorsal Horn ◽  
Cannabinoid Receptor 1 ◽  
Sarcoma Cells

Background Bone cancer pain has a strong impact on the quality of life of patients, but it is difficult to treat. Therefore, development of a novel strategy for the treatment of bone cancer pain is needed for improvement of patient quality of life. This study examined whether selective spinal cannabinoid receptor 1 (CB1) activation alleviates bone cancer pain and also examined the spinal expression of CB1. Methods A bone cancer pain model was made by implantation of sarcoma cells into the intramedullary space of the mouse femur. In behavioral experiments, the authors examined the effects of activation of spinal CB1 and inhibition of metabolism of endocannabinoid on bone cancer-related pain behaviors. Immunohistochemical experiments examined the distribution and localization of CB1 in the superficial dorsal horn of the spinal cord using specific antibodies. Results Spinal CB1 activation by exogenous administration of a CB1 agonist arachidonyl-2-chloroethylamide reduced bone cancer-related pain behaviors, including behaviors related to spontaneous pain and movement-evoked pain. In immunohistochemical experiments, although mu-opioid receptor 1 expression was reduced in the superficial dorsal horn ipsilateral to the site of implantation of sarcoma cells, CB1 expression was preserved. In addition, CB1 was mainly expressed in the axon terminals, but not in the dendritic process in the superficial dorsal horn. Conclusion Spinal CB1 activation reduced bone cancer-related pain behavior. Presynaptic inhibition may contribute to the analgesic effects of spinal CB1 activation. These findings may lead to novel strategies for the treatment of bone cancer pain.

scholarly journals Neurophysiological Mechanisms Related to Pain Management in Bone Tumors

2020 ◽  
Vol 18 ◽  
Author(s):  
Pablo Romero-Morelos ◽  
Erika Ruvalcaba-Paredes ◽  
David Garciadiego-Cázares ◽  
Martín PérezSantos ◽  
Samuel Reyes-Long ◽  
...  
Keyword(s):  
Quality Of Life ◽  
Pain Management ◽  
Cancer Pain ◽  
Bone Tumors ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Peripheral Sensitization ◽  
Related Factor ◽  
Common Symptom

Background: Primary and metastatic bone tumor incidence has increased in the last years. Pain is a common symptom and is one of the most important related factor to the decrease of quality of life in these patients. Different pain management strategies are not completely effective and many patients afflicted by cancer pain cannot be controlled properly. In this sense we need to elucidate the neurophysiology of cancer-induced pain contemplating other quality of life components such as inflammation, neuropathies and cognitive components regarding bone tumors, and thus pave the way for novel therapeutic approaches in this field. Aim: Identify the neurophysiology of the mechanisms related to pain management in bone tumors. Method: Advanced searches were performed in scientific databases: PubMed, ProQuest, EBSCO, and the Science Citation index to get information about the neurophysiology mechanisms related to pain management in bone tumors. Results: The central and peripheral mechanisms that promote bone cancer pain are poorly understood. Studies have shown that bone cancer could be related to neurochemicals produced by tumor and inflammatory cells, coupled with peripheral sensitization due to nerve compression and injury caused by tumor growth. Activity of mesolimbic dopaminergic neurons, substance P, cysteine/glutamate antiporter, and other neurochemical dynamic’s brings us putative strategies to suggest better and efficient treatments against pain in cancer patients. Conclusion: Cancer-induced bone pain could include neuropathic and inflammatory pain, but with different modifications to the periphery tissue, nerves and neurochemical changes in different neurological levels. In this sense, here we explore opportunity areas in pharmacological and non-pharmacological pain management, according to pain-involved mechanisms.

scholarly journals Preconditioning with hydrogen sulfide prevents bone cancer pain in rats through a proliferator-activated receptor gamma/p38/Jun N-terminal kinase pathway

2017 ◽  
Vol 243 (1) ◽  
pp. 57-65 ◽  
Author(s):  
Li Zhuang ◽  
Ke Li ◽  
Gaowei Wang ◽  
Tao Shou ◽  
Chunlin Gao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cancer Pain ◽  
Rat Model ◽  
Mechanical Allodynia ◽  
Antinociceptive Effect ◽  
Thermal Hyperalgesia ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Kinase Pathway

Bone cancer pain (BCP) is a severe type of hyperpathic pain occurring with primary bone tumors or advanced cancers which metastasize to bones. BCP can detrimentally reduce quality of life and presents a challenge to modern medicine. Studies have shown that exogenous H2S may act as a neuroprotectant to protect against some diseases in central nervous system. The preset study aimed to investigate the antinociceptive effect of H2S in BCP. We first measured the changes of serum H2S in patients with BCP and analyzed the relationship between them, then investigated the effect of H2S preconditioning on BCP, and explored the mechanism in rat model. Our results revealed that serum H2S level was negatively correlated with pain scores. In the rat model of BCP, preconditioning with H2S significantly reduced BCP, demonstrated by the decrease of thermal hyperalgesia and mechanical allodynia. The mechanism of H2S preconditioning may involve microglia deactivation and inflammation inhibition in the spinal cord, in which the proliferator-activated receptor gamma/p38/Jun N-terminal kinase pathway is activated. Impact statement Bone cancer pain (BCP) significantly decreases the life quality of patients or their life expectancy and causes a severe health burden to the society. However, as the exact mechanism of BCP is still poorly understood, no effective treatment has been developed yet. There are some pain medicines now, but they have some inevitable side effects. Additional therapeutic strategies are urgently needed. First, we revealed that preconditioning with H2S significantly reduced BCP, demonstrated by the decrease of thermal hyperalgesia and mechanical allodynia. Second, the mechanism of H2S preconditioning was elucidated. It may involve microglia deactivation and inflammation inhibition in the spinal cord, in which the proliferator-activated receptor gamma/p38/Jun N-terminal kinase pathway is activated. This novel finding may significantly help us to understand the difference between the roles of endogenous H2S and exogenous H2S in the development of BCP and present us a new strategy of pain management.

Connexin 43 Mediates CXCL12 Production from Spinal Dorsal Horn to Maintain Bone Cancer Pain in Rats

2015 ◽  
Vol 41 (5) ◽  
pp. 1200-1208 ◽  
Author(s):  
Li-Hua Hang ◽  
Shu-Na Li ◽  
Hong Luo ◽  
Wei-Wei Shu ◽  
Zu-Min Mao ◽  
...  
Keyword(s):  
Cancer Pain ◽  
Dorsal Horn ◽  
Connexin 43 ◽  
Spinal Dorsal Horn ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Spinal Dorsal

The bone cancer pain induced expression of NR1 and NOS on the dorsal horn of murine spinal cord

2008 ◽  
Vol 32 (3) ◽  
pp. S65-S66
Author(s):  
Dong Huang ◽  
Shai Hong Zhu ◽  
Xiao Ling Huang ◽  
Jing Song Zeng ◽  
Yong Hong Gu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cancer Pain ◽  
Dorsal Horn ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Induced Expression

scholarly journals Neuroligins Facilitate The Development of Bone Cancer Pain via Regulating Synaptic Transmission

2021 ◽  
Author(s):  
Xianqiao Xie ◽  
Yang Li ◽  
Shanchun Su ◽  
Xiaohui Li ◽  
Xueqin Xu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Chronic Pain ◽  
Cancer Pain ◽  
Dorsal Horn ◽  
Spinal Dorsal Horn ◽  
Bone Cancer ◽  
Bone Cancer Pain ◽  
Rat Spinal Cord ◽  
Spinal Dorsal

Abstract Background The underlying mechanism of chronic pain involves the plasticity in synaptic receptors and neurotransmitters. This study aimed to investigate potential roles of neuroligins (NLs) within the spinal dorsal horn of rats in a newly established bone cancer pain (BCP) model. Methods Using our rat BCP model, we assessed pain hypersensitivity over time. Quantitative real-time polymerase chain reaction and Western blot analysis were performed to investigate NL expression, and NLs were overexpressed in the rat spinal cord using lentiviral vectors. Immunofluorescence staining and whole-cell patch-clamp recordings were deployed to investigate the role of NLs in the development of BCP. Results We observed reduced expression levels of NL1 and NL2, but not NL3, within the rat spinal cord, which were found to be associated with and essential for the development of BCP in our model. Accordingly, NL1 or NL2 overexpression in the spinal cord alleviated mechanical hypersensitivity of rats. Electrophysiological experiments indicated that NL1 and NL2 are involved in BCP via regulating γ-aminobutyric acid-ergic interneuronal synapses and the activity of glutamatergic interneuronal synapses, respectively. Conclusions Our observations unravel the role of NLs in cancer-related chronic pain and further suggest that inhibitory mechanisms are central features of BCP in the spinal dorsal horn. These results provide a new perspective and basis for subsequent studies elucidating the onset and progression of BCP.

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