In rats, 2–3 weeks after peripheral nerve injury, selective blockade or knockdown of GLT-1 in the LC abolishes the effects of gabapentin on glutamate levels and hypersensitivity [39,43], suggesting that GLT-1-mediated glutamate release from astrocytes is essential to the analgesic effects of gabapentin. The gene discussed is SLC1A2; the disease is peripheral nerve injury.