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. 2010 Nov;151(2):460-466.
doi: 10.1016/j.pain.2010.08.004. Epub 2010 Aug 25.

Neuropathic pain-like alterations in muscle nociceptor function associated with vibration-induced muscle pain

Xiaojie Chen  1 , Paul G Green, Jon D Levine
Affiliations

Neuropathic pain-like alterations in muscle nociceptor function associated with vibration-induced muscle pain

Xiaojie Chen et al. Pain. 2010 Nov.

Abstract

We recently developed a rodent model of the painful muscle disorders induced by occupational exposure to vibration. In the present study we used this model to evaluate the function of sensory neurons innervating the vibration-exposed gastrocnemius muscle. Activity of 74 vibration-exposed and 40 control nociceptors, with mechanical receptive fields in the gastrocnemius muscle, were recorded. In vibration-exposed rats ∼15% of nociceptors demonstrated an intense and long-lasting barrage of action potentials in response to sustained suprathreshold mechanical stimulation (average of 2635 action potentials with frequency of ∼44Hz during a 1min suprathreshold stimulus) much greater than that has been reported to be produced even by potent inflammatory mediators. While these high-firing nociceptors had lower mechanical thresholds than the remaining nociceptors, exposure to vibration had no effect on conduction velocity and did not induce spontaneous activity. Hyperactivity was not observed in any of 19 neurons from vibration-exposed rats pretreated with intrathecal antisense for the IL-6 receptor subunit gp130. Since vibration can injure peripheral nerves and IL-6 has been implicated in painful peripheral neuropathies, we suggest that the dramatic change in sensory neuron function and development of muscles pain, induced by exposure to vibration, reflects a neuropathic muscle pain syndrome.

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Figures

Figure 1
Figure 1
a) The response of nociceptors to sustained (60 sec) (10 g) stimuli, showing individual fibers (main figure) and mean values (inset) in naïve and vibration-exposed rats. The responses of the nociceptors from the group exposed to vibration (n = 74) were significantly higher than those of control rats (n = 40, P=0.014, Student’s t-test). An unexpected group of fibers with >1500 spikes/60 s, suggest the emergence of an unusually high-firing frequency population of nociceptors in vibration-exposed rats. b) The high-firing nociceptors (>1500 spikes/60 s) in vibration-exposed rats had an ~10-fold higher number of action potentials compared to nociceptors from control rats (2635±349 vs. 216.8±49), and non-high-firing nociceptors (<1500 spikes/60s) in the vibration-exposed rats (282.5±38.7). There was no significant difference in response of neurons to suprathreshold stimulation in control and non-high-firing frequency nociceptors from vibrated rats (P=0.298). c) Single-unit C-fiber recordings of action potentials evoked by a 10-g stimulus in control and high-firing nociceptors in vibration-exposed rats.
Figure 2
Figure 2
The time course of the average responses of nociceptors during the 60 s suprathreshold stimulation, for naïve, normal and high-firing nociceptors; bin width is 1 sec.
Figure 3
Figure 3
a) While the mechanical thresholds of muscle nociceptors in control and normal firing frequency vibration-exposed rats was not significantly different, high-firing nociceptors in vibrated rats had significantly lower mechanical threshold than normal firing frequency nociceptors from vibrated rats, or nociceptors from control rats (P<0.001, one-way ANOVA). b) Scattergram of the mechanical thresholds for individual muscle nociceptors.
Figure 4
Figure 4
A. Injection of ODN antisense, but not mismatch for the gp130 subunit of the IL-6 receptor significantly reduced the magnitude of vibration-induced mechanical hyperalgesia comparison to rats receiving mismatch ODN. B. In animals pretreated with gp130 antisense, no high-firing frequency nociceptors were observed in response to a sustained (60s) suprathreshold (10 g) stimulation (P<0.05, one-tailed Chi squared).
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