Fig. 7.  PKA-dependent AMPAR surface insertion mediates N -methyl-d-aspartate (NMDA) receptor–elicited spinal reflex potentiation. (A , B ) When compared with vehicle solution (Veh, n = 7), intrathecal NMDA (10 μM, 10 μl; n = 7) induced reflex potentiation in external urethra sphincter electromyogram activity by increasing spike count (24.1 ± 4.8 spikes/stimulation, **P < 0.001). This process was prevented by pretreatment with intrathecal d-2-amino-5-phosphonovalerate (10 μM, 10 μl [APV]; 2.8 ± 0.4 spikes/stimulation, ## P < 0.001) and MDL-12330A (10 μM, 10 μl [MDL]; 7.5 ± 1.8 spikes/stimulation, ## P < 0.001). (C , D ) Immunoblotting showed that, when compared with protein levels in animals that received vehicle solution (n = 4), intrathecal NMDA caused rapid increase in phosphorylated Glu receptor 1 subunit serine 845 residue (pGluR1S845) in total lysate (*P = 0.019) as well as GluR1 (**P = 0.003) and AKAP (*P = 0.034) expression in membrane fractions (P2). This process was prevented by APV (## P = 0.004 in GluR1, # P = 0.017 in pGluR1, # P = 0.027 in AKAP vs.  TS + NMDA, n = 4) and MDL-12330A (# P = 0.026 in GluR1, P = 0.020 in pGluR1, P = 0.042 in AKAP). AMPAR =α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionate receptors; AKAP = PKA-A kinase–anchoring protein; EUSE = external urethra sphincter electromyogram; PKA = protein kinase A; sec = seconds; test stimulation = TS; uV =μvolts.