Abstract
Network states are often determined by modulators that alter the synaptic and cellular properties of the constituent neurons. Frequently neuromodulators act via second messengers, consequently their effects can persist. This persistence at the cellular/molecular level determines the maintenance of the state at the network level. Here we study a feeding network in Aplysia. In this network, persistent modulation supports the maintenance of an ingestive state, biasing the network to generate ingestive motor programs. Neuropeptides that exert cyclic adenosine monophosphate (cAMP) dependent effects play an important role in inducing the ingestive state. Most commonly, modulatory effects exerted through cAMP signaling are persistent as a consequence of PKA activation. This is not the case in the neurons we study. Instead maintenance of the network state depends on the persistence of cAMP itself. Data strongly suggest that this is a consequence of the direct activation of a cyclic nucleotide gated current.
Highlights
Second messenger signaling is a fundamental mechanism in the modulation of neural networks
The present findings demonstrating that induction of a cyclic nucleotide gated current can induce a persistent excitability increase, and thereby alter network state, are likely to be of broad interest
To determine whether PKA activation is necessary for the induction of ingestive priming one of the two B48 neurons was injected with Protein Kinase Inhibitor (PKI)[20]
Summary
Second messenger signaling is a fundamental mechanism in the modulation of neural networks. We study the network that mediates feeding behavior in the mollusc Aplysia This network is like many others in that its activity is configured and reconfigured by modulatory neurotransmitters to generate ingestive and egestive motor programs[10]. Previous work established that these increases are primarily due to an FCAP + CP2-induced increase in excitability that persists for at least fifteen minutes[16]. This persistent state is not induced in the presence of cAMP antagonists, so it is clearly cAMP-dependent[12]. The present findings demonstrating that induction of a cyclic nucleotide gated current can induce a persistent excitability increase, and thereby alter network state, are likely to be of broad interest
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