Fig. 3.  Anchorage of A kinase–anchoring proteins (AKAP) to protein kinase A and activation of the Glu receptor 1 subunits (GluR1) mediates protein kinase A–dependent reflex potentiation. (A ) Intrathecal 8-bromo-cyclic adenosine monophosphate (cAMP; 300 μM, 10 μl; test stimulation [TS]+ cAMP), but not vehicle solution (Veh; n = 7), induced reflex potentiation in external urethra sphincter electromyogram activity by significantly increasing mean spike count evoked by TS (*P = 0.019). This effect was abolished by pretreatment with intrathecal N -[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide (H89; # P = 0.024), human thyroid A kinase–anchoring protein (Ht31; # P = 0.001), and philanthotoxin-74 (PT74, 10 μM, 10 μl; P = 0.034). (B , C ) Compared with vehicle solution (n = 4), intrathecal cAMP up-regulated the expression of phosphorylated Glu receptor 1 subunit serine 845 residue (pGluR1 s845) in total lysate (*P = 0.036) as well as GluR1 (*P = 0.016) and AKAP (*P = 0.032) in the membrane fraction (P2) of lumbosacral (L6–S2) dorsal horn neurons. This process was reversed by pretreatment with H89 (## P = 0.007 in GluR1, # P = 0.046 in pGluR1, # P = 0.020 in AKAP vs.  TS + cAMP, n = 4), Ht31 (## P = 0.018 in GluR1, ## P = 0.036 in pGluR1, ## P = 0.004 in AKAP), but not PT74 (P = 0.845 in GluR1, P = 0.231 in pGluR1, P = 0.483 in AKAP). EUSE = external urethra sphincter electromyogram; sec = seconds; uV =μvolts.