Nociceptive sensitization and BDNF up-regulation in a rat model of traumatic brain injury

• Mild TBI was induced in rats using fluid percussion.
• Nociceptive assessment demonstrated little change in hindpaw thermal thresholds.
• Mild TBI rats did demonstrate mechanical allodynia contralateral to the TBI lesions.
• Lumbar spinal cord levels of BDNF were elevated contralateral to TBI at both the mRNA and protein levels.

Chronic pain after traumatic brain injury (TBI) is very common, but the mechanisms linking TBI to pain experienced in the periphery have not been described. In this set of studies we examined nociceptive sensitization and changes in spinal cord gene expression using the rat lateral fluid percussion model of mild TBI. We did not identify changes in thermal nociceptive thresholds in rats with mild TBI. However, mechanical allodynia in hind paws contralateral to TBI was significant and sustained. We also found that spinal cord levels of brain derived neurotrophic factor (BDNF) but not several other pain-related genes were up-regulated one week after injury. Our findings suggest that TBI-induced up-regulation of spinal BDNF levels might contribute to chronic TBI-related pain, and that the lateral fluid percussion model might be useful for exploring this relationship.