Calcium-Permeable AMPA Receptors in the Nucleus Accumbens Regulate Depression-Like Behaviors in the Chronic Neuropathic Pain State

Background Basic data are lacking regarding the efficacy and mechanisms of action of corticosteroids in neuropathic pain. Because recent studies indicate that spinal glial activation mediates the pathologic pain states, the authors sought to determine the effects of systemic and intrathecal methylprednisolone on the development and maintenance of neuropathic pain and spinal glial activation in a rat model. Methods Rats were anesthetized, and L5 and L6 spinal nerves were tightly ligated. Then, continuous infusion of systemic (4 mg x kg(-1) x day(-1)) or intrathecal (80 microg x kg(-1) x day(-1)) methylprednisolone or saline was started. Mechanical allodynia and thermal hyperalgesia were evaluated on days 4 and 7 postoperatively with von Frey and Hargreaves tests, respectively. Spinal astrocytic activation was evaluated with glial fibrillary acidic protein immunoreactivity on day 7. In other groups of rats, continuous 3-day treatment with intrathecal methylprednisolone or saline was started 7 days after spinal nerve ligation, when neuropathic pain had already developed. Behavioral tests and immunostaining were performed up to 3 weeks after the treatment. Results Spinal nerve ligation induced mechanical allodynia and thermal hyperalgesia on days 4 and 7 postoperatively. Glial fibrillary acidic protein immunoreactivity was remarkably enhanced on day 7. Both systemic and intrathecal methylprednisolone inhibited the development of neuropathic pain states and glial activation. Three-day treatment with intrathecal methylprednisolone reversed existing neuropathic pain state and glial activation up to 3 weeks after the treatment. Conclusion : Systemic and intrathecal methylprednisolone inhibited spinal glial activation and the development and maintenance of a neuropathic pain state in a rat model of spinal nerve ligation.

Download Full-text

TMS for Persistent Post Traumatic Brain Injury Headache-A neuropathic Pain State

Brain Stimulation ◽

10.1016/j.brs.2021.10.470 ◽

2021 ◽

Vol 14 (6) ◽

pp. 1730

Author(s):

Albert Leung

Keyword(s):

Traumatic Brain Injury ◽

Neuropathic Pain ◽

Brain Injury ◽

Pain State ◽

Post Traumatic ◽

Neuropathic Pain State

Download Full-text

Faculty Opinions recommendation of Cortical neurostimulation for neuropathic pain: state of the art and perspectives.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726089351.793533257 ◽

2017 ◽

Author(s):

Marcin Chwistek

Keyword(s):

Neuropathic Pain ◽

State Of The Art ◽

Pain State ◽

Neuropathic Pain State

Download Full-text

From the bench to the bedside: Medulloblastoma subtypes, cholinergic neuron function in the nucleus accumbens, and mechanisms of chronic neuropathic pain

Surgical Neurology International ◽

10.4103/2152-7806.76718 ◽

2011 ◽

Vol 2 (1) ◽

pp. 16

Author(s):

JasonS Hauptman

Keyword(s):

Neuropathic Pain ◽

Nucleus Accumbens ◽

Cholinergic Neuron ◽

Chronic Neuropathic Pain ◽

Neuron Function

Download Full-text

Albiflorin Attenuates Mood Disorders Under Neuropathic Pain State by Suppressing the Hippocampal NLRP3 Inflammasome Activation During Chronic Constriction Injury

The International Journal of Neuropsychopharmacology ◽

10.1093/ijnp/pyaa076 ◽

2020 ◽

Author(s):

Pei Liu ◽

Jianjun Chen ◽

Shuai Ma ◽

Jianjun Zhang ◽

Jianyu Zhou

Keyword(s):

Neuropathic Pain ◽

Mood Disorders ◽

Nlrp3 Inflammasome ◽

Chronic Constriction Injury ◽

Anxiety And Depression ◽

Inflammasome Activation ◽

Nuclear Factor ◽

Nlrp3 Inflammasome Activation ◽

Pain State ◽

Neuropathic Pain State

Abstract Background Neuropathic pain is a multifaceted and ubiquitous disease across the globe. Mood disorders, such as anxiety and depression, are frequently observed in patients suffering from neuropathic pain. Both neuropathic pain and comorbid mood disorders seriously impact quality of life. Accumulated evidence shows that activation of the NOD-like receptor protein 3 (NLRP3) inflammasome is involved in the neuroinflammatory pathogenesis of neuropathic pain, anxiety, and depression. However, the role of the NLRP3 inflammasome in the pathological process of anxiety and depression under the neuropathic pain state has not been fully described. Albiflorin, a monoterpene glycoside, may be a potential regulator of the NLRP3 inflammasome, but it is not clear whether albiflorin relates to NLRP3 inflammasome activation. Methods We used a systematic pharmacological method to confirm whether the activation of the NLRP3 inflammasome in the hippocampus was involved in the development of neuropathic pain associated with mood disorders and whether albiflorin could be an effective treatment for these symptoms. Results The NLRP3 inflammasome contributed to the neuropathic pain and comorbid anxiety and depression-like behaviors induced by chronic constriction injury of the sciatic nerve, and albiflorin may relieve these symptoms via inhibition of the NLRP3 inflammasome activity. Moreover, albiflorin enhanced the translocation of the nuclear factor erythroid 2-related factor 2 into the nucleus and suppressed nuclear factor-kappa B activity in the hippocampus. Conclusions Albiflorin, as a potential therapeutic agent, might greatly improve the overall symptoms of neuropathic pain.

Download Full-text