ABSTRACT
Background
Neuropathic pain (NP) after spinal cord injury (SCI) is a disabling condition, without an effective treatment. Hyperexcitability of N‐methyl‐D‐aspartate (NMDA) receptors and oxidative stress have been reported to be associated with pain development. Amantadine, a NMDA receptor antagonist, has been proposed as a potential therapy for NP. However, its use has not been tested for NP after SCI.
Methods
In order to produce SCI, 120 female Wistar rats were used, a contusion injury to the T10 and T12 thoracic vertebrae was performed from heights of 6.25 mm and 12.5 mm. Nociceptive behavior, was evaluated with the use of von Frey filaments for 31 days. The final products of lipid peroxidation (LP) and concentration of reduced glutathione (GSH) in the injured tissue were quantified by fluorescence spectrophotometry. The antinociceptive effect of the acute (15 days after the injury) and chronic (once daily for three days immediately after the injury) with amantadine (6.25‐50 mg/Kg. I.p.) was determined. Finally, the LP and GSH were quantified in the injured tissue.
Results
Acute treatment with amantadine reduced nociceptive behavior. Concomitantly, LP was decreased by Amantadine treatment while GSH increased in the injured tissue. Similar effects were observed with chronic treatment with amantadine.
Conclusions
Data from this study suggested that the antinociceptive effects of amantadine treatment are modulated through oxidative stress and excitotoxicity reduction associated to N‐methyl‐D‐aspartate receptors activation.
from Wiley: European Journal of Pain: Table of Contents https://ift.tt/3uN0exw
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