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Voluntary Exercise Training: Analysis of Mice in Uninjured, Inflammatory, and Nerve-Injured Pain States.

Sheahan TD, Copits BA, Golden JP, Gereau RW - PLoS ONE (2015)

Bottom Line: In uninjured, adult C57BL/6J mice, 1 to 4 weeks of exercise training did not alter nociceptive thresholds, lumbar dorsal root ganglia neuronal excitability, or hindpaw intraepidermal innervation.Lastly, 2 weeks of exercise training was ineffective in reversing spared nerve injury-induced mechanical hypersensitivity or in improving muscle wasting or hindpaw denervation.These findings indicate that in contrast to rodent forced exercise paradigms, short durations of voluntary wheel running do not improve pain-like symptoms in mouse models of acute inflammation and peripheral nerve injury.

View Article: PubMed Central - PubMed

Affiliation: Washington University Pain Center and Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri, United States of America; Washington University Program in Neuroscience, Washington University School of Medicine, St. Louis, Missouri, United States of America.

ABSTRACT
Both clinical and animal studies suggest that exercise may be an effective way to manage inflammatory and neuropathic pain conditions. However, existing animal studies commonly use forced exercise paradigms that incorporate varying degrees of stress, which itself can elicit analgesia, and thus may complicate the interpretation of the effects of exercise on pain. We investigated the analgesic potential of voluntary wheel running in the formalin model of acute inflammatory pain and the spared nerve injury model of neuropathic pain in mice. In uninjured, adult C57BL/6J mice, 1 to 4 weeks of exercise training did not alter nociceptive thresholds, lumbar dorsal root ganglia neuronal excitability, or hindpaw intraepidermal innervation. Further, exercise training failed to attenuate formalin-induced spontaneous pain. Lastly, 2 weeks of exercise training was ineffective in reversing spared nerve injury-induced mechanical hypersensitivity or in improving muscle wasting or hindpaw denervation. These findings indicate that in contrast to rodent forced exercise paradigms, short durations of voluntary wheel running do not improve pain-like symptoms in mouse models of acute inflammation and peripheral nerve injury.

No MeSH data available.


Related in: MedlinePlus

Exercise training did not alter DRG neuron membrane or excitability properties of uninjured animals.Whole-cell patch clamp electrophysiology was performed on small-diameter cultured lumbar DRG neurons, N = 2–3 animals. (A) An example of a patched neuron approximately 23 μm in diameter. (B) Resting membrane potential was unaltered by exercise training for 1, 2 or 4 weeks, n = 13–25. Representative traces of action potentials elicited by step (C) and ramp (D) current injections of 1 to 3 times rheobase. A negative stepwise current was used to determine input resistance (Rin). Scale bars represent 20 mV and 100 ms. Rheobase in response to both step (E) and ramp (F) current injection was also unchanged by exercise, n = 13–25 and 7–23, respectively. The number of action potentials elicited by step (G) and ramp (H) current injections 2 and 3 times rheobase was unaffected by 4 weeks of exercise training, n = 22–25 and 20–23, respectively. Data are presented as mean ± SEM. Student’s t-Test, Bonferroni correction for multiple comparisons.
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pone.0133191.g002: Exercise training did not alter DRG neuron membrane or excitability properties of uninjured animals.Whole-cell patch clamp electrophysiology was performed on small-diameter cultured lumbar DRG neurons, N = 2–3 animals. (A) An example of a patched neuron approximately 23 μm in diameter. (B) Resting membrane potential was unaltered by exercise training for 1, 2 or 4 weeks, n = 13–25. Representative traces of action potentials elicited by step (C) and ramp (D) current injections of 1 to 3 times rheobase. A negative stepwise current was used to determine input resistance (Rin). Scale bars represent 20 mV and 100 ms. Rheobase in response to both step (E) and ramp (F) current injection was also unchanged by exercise, n = 13–25 and 7–23, respectively. The number of action potentials elicited by step (G) and ramp (H) current injections 2 and 3 times rheobase was unaffected by 4 weeks of exercise training, n = 22–25 and 20–23, respectively. Data are presented as mean ± SEM. Student’s t-Test, Bonferroni correction for multiple comparisons.

Mentions: Increased excitability of DRG neurons has been shown to underlie hypersensitivity in a number of pain states [46–48]. To determine whether exercise affects membrane and cell excitability properties in an uninjured context, whole-cell patch clamp electrophysiology was performed on dissociated L3-L5 DRG neuron cultures obtained from exercise trained and control animals within 24 hr of culturing (Fig 2A). Recordings were performed on small diameter neurons ranging from 20–30 μm to increase the likelihood of recording from nociceptive neurons.


Voluntary Exercise Training: Analysis of Mice in Uninjured, Inflammatory, and Nerve-Injured Pain States.

Sheahan TD, Copits BA, Golden JP, Gereau RW - PLoS ONE (2015)

Exercise training did not alter DRG neuron membrane or excitability properties of uninjured animals.Whole-cell patch clamp electrophysiology was performed on small-diameter cultured lumbar DRG neurons, N = 2–3 animals. (A) An example of a patched neuron approximately 23 μm in diameter. (B) Resting membrane potential was unaltered by exercise training for 1, 2 or 4 weeks, n = 13–25. Representative traces of action potentials elicited by step (C) and ramp (D) current injections of 1 to 3 times rheobase. A negative stepwise current was used to determine input resistance (Rin). Scale bars represent 20 mV and 100 ms. Rheobase in response to both step (E) and ramp (F) current injection was also unchanged by exercise, n = 13–25 and 7–23, respectively. The number of action potentials elicited by step (G) and ramp (H) current injections 2 and 3 times rheobase was unaffected by 4 weeks of exercise training, n = 22–25 and 20–23, respectively. Data are presented as mean ± SEM. Student’s t-Test, Bonferroni correction for multiple comparisons.
© Copyright Policy
Related In: Results  -  Collection

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Show All Figures
getmorefigures.php?uid=PMC4510282&req=5

pone.0133191.g002: Exercise training did not alter DRG neuron membrane or excitability properties of uninjured animals.Whole-cell patch clamp electrophysiology was performed on small-diameter cultured lumbar DRG neurons, N = 2–3 animals. (A) An example of a patched neuron approximately 23 μm in diameter. (B) Resting membrane potential was unaltered by exercise training for 1, 2 or 4 weeks, n = 13–25. Representative traces of action potentials elicited by step (C) and ramp (D) current injections of 1 to 3 times rheobase. A negative stepwise current was used to determine input resistance (Rin). Scale bars represent 20 mV and 100 ms. Rheobase in response to both step (E) and ramp (F) current injection was also unchanged by exercise, n = 13–25 and 7–23, respectively. The number of action potentials elicited by step (G) and ramp (H) current injections 2 and 3 times rheobase was unaffected by 4 weeks of exercise training, n = 22–25 and 20–23, respectively. Data are presented as mean ± SEM. Student’s t-Test, Bonferroni correction for multiple comparisons.
Mentions: Increased excitability of DRG neurons has been shown to underlie hypersensitivity in a number of pain states [46–48]. To determine whether exercise affects membrane and cell excitability properties in an uninjured context, whole-cell patch clamp electrophysiology was performed on dissociated L3-L5 DRG neuron cultures obtained from exercise trained and control animals within 24 hr of culturing (Fig 2A). Recordings were performed on small diameter neurons ranging from 20–30 μm to increase the likelihood of recording from nociceptive neurons.

Bottom Line: In uninjured, adult C57BL/6J mice, 1 to 4 weeks of exercise training did not alter nociceptive thresholds, lumbar dorsal root ganglia neuronal excitability, or hindpaw intraepidermal innervation.Lastly, 2 weeks of exercise training was ineffective in reversing spared nerve injury-induced mechanical hypersensitivity or in improving muscle wasting or hindpaw denervation.These findings indicate that in contrast to rodent forced exercise paradigms, short durations of voluntary wheel running do not improve pain-like symptoms in mouse models of acute inflammation and peripheral nerve injury.

View Article: PubMed Central - PubMed

Affiliation: Washington University Pain Center and Department of Anesthesiology, Washington University School of Medicine, St. Louis, Missouri, United States of America; Washington University Program in Neuroscience, Washington University School of Medicine, St. Louis, Missouri, United States of America.

ABSTRACT
Both clinical and animal studies suggest that exercise may be an effective way to manage inflammatory and neuropathic pain conditions. However, existing animal studies commonly use forced exercise paradigms that incorporate varying degrees of stress, which itself can elicit analgesia, and thus may complicate the interpretation of the effects of exercise on pain. We investigated the analgesic potential of voluntary wheel running in the formalin model of acute inflammatory pain and the spared nerve injury model of neuropathic pain in mice. In uninjured, adult C57BL/6J mice, 1 to 4 weeks of exercise training did not alter nociceptive thresholds, lumbar dorsal root ganglia neuronal excitability, or hindpaw intraepidermal innervation. Further, exercise training failed to attenuate formalin-induced spontaneous pain. Lastly, 2 weeks of exercise training was ineffective in reversing spared nerve injury-induced mechanical hypersensitivity or in improving muscle wasting or hindpaw denervation. These findings indicate that in contrast to rodent forced exercise paradigms, short durations of voluntary wheel running do not improve pain-like symptoms in mouse models of acute inflammation and peripheral nerve injury.

No MeSH data available.


Related in: MedlinePlus