Transition to endogenous bursting after long-term decentralization requires De novo transcription in a critical time window.

Rhythmic motor pattern generation by the pyloric network in the lobster stomatogastric ganglion (STG) requires neuromodulatory inputs from adjacent ganglia. However, although suppression of these inputs by cutting the stomatogastric nerve (stn) causes the pyloric network to fall silent, network output similar to that expressed when the stn is intact returns after 3-4 days in organ culture. Intracellular recordings from identified pyloric dilator (PD) neurons indicate that the fundamental change underlying rhythm recovery resides with the intrinsic excitability of pyloric neurons themselves, since the prolonged absence of extrinsic modulatory inputs allows the expression of an endogenous oscillatory capability that is maintained in a strictly conditional state when these inputs are present. To examine whether gene transcription was involved in this change in neuronal behavior, we performed in vitro experiments in which the STG was exposed to the RNA-synthesis inhibitor actinomycin D (ACD). ACD (50 microM) incubation at the time of decentralization prevented subsequent reacquisition of PD neuron bursting, but the inhibitor was much less effective when applied at later postdecentralization times, suggesting that the recovery process arises from new protein synthesis triggered when modulatory inputs are first removed. Moreover, in the nondecentralized STG, trans-synaptic modulatory instruction may sustain the conditional pyloric network phenotype by continuously regulating expression of genes responsible for intrinsic neuronal rhythmogenesis.