The loss of GABAergic inhibitory interneurons correlates with the development of thermal hyperalgesia after spinal cord injury

Elimination of chronic pain is very important in improving quality of life for both paraplegics and quadriplegics alike. It is hypothesized that hyperexcitability found after injury may be attributed to a loss of GABA inhibitory control caused by the loss of GABAergic inhibitory interneurons. Transgenic mice with expression of green fluorescenct protein found in GABAergic inhibitory interneurons were used. SCI was performed at the 10th thoracic spinal segment with a spinal cord impactor. Hyperalgesia was observed at 3 weeks post injury and continued on to week 6. 6 weeks post injury there was a loss of inhibitory interneurons in lamina I-III. Gabapentin and tiagabine were administered as analgesics. Gabapentin blocked hyperalgesia by 50% at 10mg/kg while tiagabine blocked hyperalgesia by 50% at 1mg/kg and completely blocked it at 10mg/kg. Enhancing GABAergic signalling decreases hyperalgesia and therefore GABAergic interneurons may play a key role in the development of hyperalgesia following SCI.