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. 2009 Oct;10(10):1073-7.
doi: 10.1016/j.jpain.2009.04.005. Epub 2009 Jul 2.

Sound stress-induced long-term enhancement of mechanical hyperalgesia in rats is maintained by sympathoadrenal catecholamines

Sachia G Khasar  1 , Olayinka A Dina, Paul G Green, Jon D Levine
Affiliations

Sound stress-induced long-term enhancement of mechanical hyperalgesia in rats is maintained by sympathoadrenal catecholamines

Sachia G Khasar et al. J Pain. 2009 Oct.

Abstract

Although stress plays an important role in chronic widespread pain syndromes, such as fibromyalgia, the underlying mechanism has remained elusive. We have recently demonstrated, in a model of chronic widespread pain, that prolonged enhancement of immune mediator hyperalgesia, induced by unpredictable sound stress, requires a contribution of both the sympathoadrenal (epinephrine) and the hypothalamic-pituitary adrenal (corticosterone) neuroendocrine stress axes. Because this stress protocol produced sustained elevation of plasma epinephrine, in the current study we tested the hypothesis that the sympathoadrenal axis also plays a role in maintenance of symptoms in this model of chronic widespread pain. After establishment, adrenal medullectomy abolished the enhancement of epinephrine-induced cutaneous and muscle hyperalgesia. Administration of stress levels of epinephrine to adrenal medullectomized rats reconstituted the pain phenotype. These observations suggest that the sympathoadrenal stress axis plays a major role in the induction as well as maintenance of stress-induced enhancement of mechanical hyperalgesia, mediated by prolonged elevation of circulating epinephrine.

Perspective: We present data showing mechanical hyperalgesia persisting for up to 28 days after exposure to sound stress, with evidence that the sympathoadrenal axis mediator epinephrine plays a major role. These findings could have clinical implications with regard to novel potential treatments for chronic widespread pain syndromes, such as fibromyalgia.

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Figures

Figure 1
Figure 1
Reversal of stress-induced enhancement of epinephrine hyperalgesia (28 d post stress, filled squares) by adrenal medullectomy (28 d post-stress, AMedX, filled triangles)) and reconstitution of the enhanced hyperalgesia (28 d post-stress, AMedX, + Epi, filled inverted triangles) by implants of epinephrine in A) the skin (dorsal aspect of the hind paw) and B) skeletal (gastrocnemius) muscle of the rat. Adrenal medullectomy, with or without epinephrine implants, was performed 14 days after the last sound stress exposure and rats were used for experiments 14 days after surgery.
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