Implication of Hypothalamus in Alleviating Spinal Cord Injury-Induced Neuropathic Pain

Crowell, Andrew; King, Kevin C; Deitermann, Annika; Miranpuri, Gurwattan S.; Resnick, Daniel K.

doi:10.1159/000449183

Cited by 5 publications

(2 citation statements)

References 32 publications

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“…Neuropathic pain is closely related to its pathophysiological state in the nervous system. 1 , 2 Research has discovered that neuropathic pain shares several similarities with other neurobiological processes, particularly with respect to the development and maintenance of pain. 3 In the past, neuropathic pain was mainly thought to be caused by spinal neuronal cell death, but this point of view has gradually become controversial.…”

Section: Introductionmentioning

confidence: 99%

Effects of hyperbaric oxygen therapy on neuropathic pain via mitophagy in microglia

Han

Liu

et al. 2017

Mol Pain

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PurposeHyperbaric oxygen (HBO) therapy has been suggested to palliate neuropathic pain, but the mechanisms involved are not well understood. This study explored the involvement of microglial mitophagy via HBO relative to neuropathic pain therapy.Materials and methodsA total of 80 male Sprague Dawley rats were randomly divided into two groups: a normal group (n = 40) and a mitophagy inhibitor group (n = 40) in which the mitophagy inhibitor cyclosporin A (CsA) was administrated prior to chronic constriction injury (CCI). Groups (n = 10 rats per group) consisted of the following: control (C), sham operation (S), sciatic nerve with chronic constriction injury (CCI), and a CCI plus HBO treatment (CCI + HBO). Pain-related behaviors were evaluated using mechanical withdraw tendency and thermal withdraw latency analysis. Mitochondrial membrane potential was measured, and Western blot was employed to assess expression of NIX and BNIP3. Immunofluorescence changes in neuron protein (NESTIN) and mitochondria inner or outer layer proteins (TIM23, TOM20) were examined.ResultsHBO significantly ameliorated pain-related behaviors, which were downregulated by mitophagy inhibitors (P < 0.05). Mitochondrial membrane potential indexes were decreased after HBO therapy, but were reversed in the mitophagy inhibitor group (P < 0.05). HBO upregulated NIX and BNIP3 expression, which did not occur in the CCI group (P < 0.05). However, expression was reduced when mitophagy inhibitors were administered. Immunofluorescence examination showed that mitophagy in microglia was induced by CCI, which was upregulated after HBO treatment. This phenomenon was not observed in the mitophagy inhibitor group.ConclusionsHBO therapy palliated CCI-induced neuropathic pain in rats by upregulating microglial mitophagy. These results could serve as guidelines to improve neuropathic pain therapy using HBO to maximize therapeutic efficiency.

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Section: Introductionmentioning

confidence: 99%

Effects of hyperbaric oxygen therapy on neuropathic pain via mitophagy in microglia

Han

Liu

et al. 2017

Mol Pain

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“…In particular, it was recently proposed that FM may involve localized inflammation in the hypothalamus [ 26 ]. Indeed, some chronic pain conditions, including fibromyalgia, have been directly linked to abnormalities in the hypothalamus–pituitary–adrenal axis (HPA) [ 45 ]. In addition, regulation of nociceptive input originates in the hypothalamus and is transmitted to the spinal cord via brain stem nuclei in the medulla [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Inhibition of P2X7 Purinergic Receptor Ameliorates Fibromyalgia Syndrome by Suppressing NLRP3 Pathway

D’Amico

Fusco

Siracusa

et al. 2021

IJMS

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Fibromyalgia is a chronic condition characterized by persistent widespread pain that significantly reduces quality of life in patients. The purinergic P2X7 receptor (P2X7R) seems to be involved in different pain states and neuroinflammation. The purpose of this study is to investigate the positive effects of P2X7R inhibition by the antagonist Brilliant Blue G (BBG) in a rat model of reserpine-induced fibromyalgia. Sprague–Dawley male rats were injected with 1 mg/kg of reserpine for three consecutive days. Later, animals were administered BBG (50 mg/kg) intraperitoneally for seven days. Reserpine injections induced a significant increase in pain pro-inflammatory mediators as well as a significant increase in neuroinflammation. Chronic pain, in turn, led to depressive-like symptoms and reduced neurogenesis. Blockage of P2X7R by BBG administrations is able to attenuate the behavioral deficits, pain mediators and microglial activation induced by reserpine injection. Additionally, BBG prevents NLRP3 inflammasome activation and consequently the release of active interleukin (IL)-1 and IL-18, involved in the activation of nociceptors. In conclusion, these results suggest that inhibition of P2X7R should be further investigated to develop a potential approach for the management of fibromyalgia.

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Spinal cord injury causes insulin resistance associated with PI3K signaling pathway in hypothalamus

Cheng

Ren

Sun

et al. 2020

Neurochemistry International

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Implication of Hypothalamus in Alleviating Spinal Cord Injury-Induced Neuropathic Pain

Cited by 5 publications

References 32 publications

Effects of hyperbaric oxygen therapy on neuropathic pain via mitophagy in microglia

Effects of hyperbaric oxygen therapy on neuropathic pain via mitophagy in microglia

Inhibition of P2X7 Purinergic Receptor Ameliorates Fibromyalgia Syndrome by Suppressing NLRP3 Pathway

Spinal cord injury causes insulin resistance associated with PI3K signaling pathway in hypothalamus

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