Figure 2.

GPR regulation of the gastric mill retractor phase is weakened by the presence of CCAP in a computational model. A, Circuit schematic representing the CCAP modulation of the GPR influence on the MCN1-activated gastric mill CPG in a compartmental model. The model is modified from the original model in the study by Nadim et al. (1998) by the addition of the indicated CCAP and GPR actions. Specifically, as in previously published models, the CCAP-activated conductance was added to the LG neurite compartment (DeLong et al., 2009a), and an inhibitory GPR synapse was added onto the passive terminal compartment of MCN1 (Beenhakker et al., 2005; DeLong et al., 2009b). The gray compartments have active properties mediated by voltage-dependent, Hodgkin–Huxley-like conductances to facilitate action potential generation, whereas the white compartments are passive. Symbols: Filled circles, Synaptic inhibition; T-bars, synaptic excitation; resistor, electrical coupling. B, GPR selectively prolongs the retractor phase of the MCN1-elicited gastric mill rhythm in the absence of CCAP. Under these conditions, the MCN1-elicited inward current (I_MI-MCN1) and associated conductance (G_MI-MCN1) in LG grew in amplitude during each retractor (LG-silent) phase because of continual MCN1 release of CabTRP Ia, and decayed during each protractor (LG-active) phase because of the LG presynaptic inhibition of MCN1_STG (Figs. 1C, 2A). As in the biological preparation, GPR stimulation during the retractor phase selectively prolonged that phase (Beenhakker et al., 2005; DeLong et al., 2009b). The fast transient events in I_MI-MCN1 resulted from the rapid changes in driving force as the LG membrane potential repeatedly approached the I_MI reversal potential during the LG action potentials (DeLong et al., 2009a). C, Adding the CCAP-activated conductance (G_MI-CCAP) to LG reduced the ability of GPR to prolong retraction. In the presence of G_MI-CCAP, the GPR stimulation was less effective in prolonging the retractor phase relative to the control condition (B). Note also that, as reported previously (Kirby and Nusbaum, 2007; DeLong et al., 2009b), G_MI-MCN1 and G_MI-CCAP exhibited different trajectories during the LG burst, and it is the sustained G_MI-CCAP amplitude during protraction (LG burst) that prolonged this phase relative to the control condition (B). As above, the fast transient events in I_MI-MCN1 and I_MI-CCAP resulted from the rapid changes in driving force during the LG action potentials.