In parallel with the hypothesis suggested above for the interaction between descending serotoninergic and spinal mechanisms of excitability modulated via the pNR1 NMDA receptor, the application of noradrenergic agonists such as clonidine has been shown to inhibit GFAP upregulation, nuclear factor-kappa B activation, and p38 mitogen-activated protein kinase induction following peripheral nerve injury [76]. The gene discussed is GFAP; the disease is peripheral nerve injury.