Exercise training modulates glutamic acid decarboxylase-65/67 expression through TrkB signaling to ameliorate neuropathic pain in rats with spinal cord injury

This study investigates whether exercise training can alleviate neuropathic pain after spinal cord injury (SCI) in rats. The researchers focused on the role of glutamic acid decarboxylase (GAD), an enzyme involved in the synthesis of GABA, a neurotransmitter that inhibits pain signals. The study examined whether exercise training could increase GAD expression in the spinal cord through tropomyosin-related kinase B (TrkB) signaling, a pathway activated by brain-derived neurotrophic factor (BDNF). The results suggest that exercise training does increase GAD expression via TrkB signaling, which helps to relieve neuropathic pain in rats with SCI. Blocking TrkB signaling eliminated the pain-relieving effects of exercise.

• 1
  Spinal cord injury leads to mechanical allodynia and thermal hyperalgesia and altered BDNF expression in rats.
• 2
  Exercise training increases the synthesis of BDNF, TrkB, CREB, p-CREB, GAD-65, and GAD-67 within the distal spinal cord of rats with SCI, and improves the mechanical withdrawal thresholds (MWTs) and thermal withdrawal latencies (TWLs).
• 3
  Blocking TrkB signaling inhibits the effects of exercise training, reducing the synthesis of CREB, p-CREB, GAD-65, and GAD-67 and the analgesic effect of exercise training was significantly inhibited.