Evidence suggests that early-stage neuroinflammation, potentially caused by acute injury, inhibits GABAAα1 expression through astrocyte activation, which subsequently downregulates the BDNF-TrkB signal pathway and results in an impairment of neurogenesis, thus affecting depression-like symptoms concurrently associated with chronic pain comorbidities [50]. This evidence concerns the gene NTRK2 and depressive symptom measurement.