Sound stress (SS) elicits behavioral changes, including
pain behaviors. However, the neuronal mechanisms underlying SS-induced
pain behaviors remain to be explored. The current study examined the effects of SS on nociceptive behaviors and changes in expression of the spinal
corticotropin-releasing factor (CRF) system in male Sprague Dawley rats with and without thermal
pain. We also studied the effects of SS on plasma
corticosterone and fecal output. Rats were exposed to 3 days of SS protocol (n = 12/group). Changes in nociceptive behaviors were assessed using thermal and mechanical
pain tests. Following the induction of SS, a subgroup of rats (n = 6/group) was inflicted with thermal injury and on day 14 postburn nociceptive behaviors were reassessed. Spinal
CRF receptor mRNA expression was analyzed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR). In addition, plasma
corticosterone and spinal CRF concentrations were quantified using
enzyme-linked
immunosorbent assay (ELISA). Increased defecation was observed in SS rats. SS produced transient
mechanical allodynia in naive rats, whereas it exacerbated thermal
pain in thermally injured rats. Spinal CRFR2
mRNA expression was unaffected by stress or thermal injury alone, but their combined effect significantly increased its expression. SS had no effect on plasma
corticosterone and spinal CRF
protein in postburn rats. To conclude, SS is capable of exacerbating postburn thermal
pain, which is linked to increased CRFR2 gene expression in the spinal cord. Future studies have to delineate whether attenuation of CRFR2 signaling at the spinal level prevents stress-induced exacerbation of
burn pain.