Fig. 7

Summary of PKA subunits regulation at the NMJ during nerve-induced muscle contraction. Model of the PKA regulation resulted from this study during nerve-induced muscle contraction. Muscle contraction opposes the presynaptic stimulation in many steps of the signaling. (1) It decreases Cβ levels maybe as a result of the activity-induced degradation of the subunit because (2) the contraction-induced upregulation of AKAP150 is capable of recruiting enough RIIβ regulatory subunits (3) to permit Cβ catalytic subunits to increase their activity enhancing pSNAP-25 T138 phosphorylation. In addition, (4) RIIα opposes to this regulation binding to Cβ to inhibit its activity contributing to balance (5) the catalytical activity of Cβ on pSynapsin-1 S9. These results indicate that bidirectional communication and balance between pre- and postsynaptic activity provide the optimal conditions to maintain the stable neurotransmission of ACh