Fig. 8.
Proposed mechanism of activation for proctolin-induced IMI. According to this model, IMI channels are activated by a neuropeptide GPCR using a pertussis toxin-sensitive pathway that is independent from a different GPCR-mediated voltage-dependence pathway (not shown; cf. Gray and Golowasch 2016). Calmodulin (CaM) via calmodulin-dependent kinases CamKII and MLCK, activated by exogenous calcium entering the cell via either the IMI channels themselves (shown) or voltage-dependent calcium channels (not shown), amplifies the activation. This is aided by a further increase in intracellular calcium level due to calcium-induced calcium release mediated by RyRs. Blunt-ended lines show agents that inhibit the indicated paths; arrows indicate activating agents and pathways. ER, endoplasmic reticulum; ProcR, proctolin receptor; RyR ryanodine receptor.