Effects of swimming exercise on neuropathic pain in a rat model: role of glutamate

ABSTRACT

Objective

The pain-reducing effects of the exercise were exerted through different mechanisms. Knowing more clear mechanisms helps to find more approach that is therapeutic. The objective of the present study is the evaluation of cerebrospinal fluid (CSF) glutamate level alteration in neuropathic pain rats and whether physical activity could modulate it.

Methods

In the present study 104 male Wistar rats weighing 180–220 g were randomly divided into 4 groups (Sham, Sham + Exe, Neuropathy, and Neuropathy + Exe) which in turn each group subdivided into 4 groups according to time points for behavioral testing and CSF sampling (Baseline, 2 weeks, 3 weeks, and 4 weeks). To induction of neuropathy (by chronic constriction injury,), after anesthetizing with a mixture of ketamine (80 mg/kg) and xylazine (10 mg/kg), the animal’s right sciatic nerve was exposed and was ligated using four movable catgut chromic suture 4/0. The exercise protocol included 25 min of daily swimming, 5 days a week for 4 weeks. Thermal hyperalgesia and mechanical tactile threshold were detected using the plantar test and Von Frey filaments, respectively. CSF glutamate level was determined using high-performance liquid chromatography.

Results

Findings indicated that mechanical and thermal thresholds significantly (p < 0.01, p < 0.05 respectively) decreased in the neuropathy group against that in sham groups. On the other hand, exercise significantly increased mechanical tactile threshold (p < 0.0012) and thermal threshold (p < 0.05) compared to the neuropathy group. Moreover, CSF glutamate level prominently (p < 0.01) was increased in the neuropathy group compared to the sham group, and swimming exercise significantly (p < 0.001) reduced it.

In conclusion

The present findings provide new evidence showing that medium-intensity swimming exercise attenuates pain-like behaviors in neuropathic pain animals, which is possibly due to decreasing CSF glutamate level and its neurotransmission.

GRAPHICAL ABSTRACT

KEYWORDS:

• Neuropathic pain
• exercise
• cerebrospinal fluid
• glutamate
• rat

Acknowledgments

The authors wish to thank the Deputy of Research and Technology of Semnan University of Medical Sciences, Semnan, Iran for offering the grants for the present investigation.

The authors of this article hereby express their gratitude to Mr. Hossein Ali Safakhah and Dr. Fatemeh Abbaszadeh for Technical assistance.

Disclosure statement

No potential conflict of interest was reported by the author(s).

Data availability statement

Supporting data that derived the findings of this study are available from the corresponding author on request.

Author’s contributions

Ali ghanbari designed the overall study.

Ali ghanbari and Sahar ghasemi and Ali Khaleghian collected data and carried out the lab work. Ali ghanbari and Ali Khaleghian carried out the statistical analysis.

Sahar ghasemi mostly drafted the manuscript.

Ali ghanbari coordinated and supervised the study.

All authors approved the manuscript.

Additional information

Funding

This work was supported by grants [IR.SEMUMS.REC.1398.137] from Semnan University of Medical Sciences.