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. 2014 Jul 15;112(2):463-6.
doi: 10.1152/jn.00034.2014. Epub 2014 Apr 30.

Does the antihyperalgesic disruptor of endothelial cells, octoxynol-9, alter nociceptor function?

Xiaojie Chen  1 , Paul G Green  1 , Jon D Levine  2
Affiliations

Does the antihyperalgesic disruptor of endothelial cells, octoxynol-9, alter nociceptor function?

Xiaojie Chen et al. J Neurophysiol. .

Abstract

The vasoactive mediator, endothelin-1, elicits a novel form of hyperalgesia, stimulation-dependent hyperalgesia. Acting on its cognate receptor on the vascular endothelial cell, endothelin-1 produces a state in which mechanical stimulation now elicits release of pronociceptive mediators from endothelium that, in turn, acts at receptors on sensory neurons. The only evidence that octoxynol-9, a surface-active agent that attenuates both endothelial cell function and stimulus-dependent hyperalgesia, does not affect nociceptors is indirect (i.e., octoxynol-9 treatment did not affect behavioral nociceptive threshold or hyperalgesia induced by agents that act directly on nociceptors). To help address the question of whether the attenuation of stimulation-dependent hyperalgesia by octoxynol-9 treatment is due to alteration of nociceptor function, we used in vivo single-fiber electrophysiological recordings. Consistent with our previous behavioral observations, we observed no significant effect of octoxynol-9 on mechanical threshold in nociceptors, their response to sustained suprathreshold mechanical stimulation, conduction velocity, and change in mechanical threshold in response to the direct-acting hyperalgesic agent, PGE2. Although octoxynol-9 did not produce a biologically meaningful change in parameters of nociceptor function, we cannot exclude the possibility of a type II error. However, our data provide preliminary evidence of no effect of octoxynol-9 on nociceptors and are consistent with the suggestion that the primary action of octoxynol-9 in our studies is due to its action on the endothelium.

Keywords: electrophysiology; endothelium; skeletal muscle; stimulus-dependent hyperalgesia.

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Figures

Fig. 1.
Fig. 1.
Mechanical threshold of nociceptors innervating the gastrocnemius muscle. Octoxynol-9 administration did not affect the baseline mechanical threshold of muscle nociceptors (A: mean; B: individual fibers).
Fig. 2.
Fig. 2.
The response of nociceptors to sustained (60-s) suprathreshold (10-g) von Frey hair mechanical stimuli in muscle nociceptors. Mean values (A) and individual fibers (B) are shown from naïve control and octoxynol-9-treated rats. The responses of the nociceptors from the octoxynol-9-treated rats were not significantly different from those of control rats for any of the analysis periods (0–10, 10–60, or 0–60 s).
Fig. 3.
Fig. 3.
Conduction velocity. A: mean conduction velocity from octoxynol-9-treated rats were not significantly different from naïve rats. B: scattergram of conduction velocities of muscle nociceptors in naïve control and octoxynol-9-treated rats.
Fig. 4.
Fig. 4.
Mechanical threshold. A: mean baseline mechanical threshold and the mechanical nociceptive threshold 25 and 55 min after PGE2 administration was not significantly different in octoxynol-9- and vehicle-treated rats. B: scattergram of mechanical nociceptive threshold of muscle nociceptors in naïve control and octoxynol-9-treated rats.
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