Functional stability and recurrent spike-timing-dependent plasticity in rhythmogenesis

Synapses in the nervous system show considerable volatility, raising the question of how the brain maintains functional stability despite continuous synaptic motility. Previous studies have suggested that functionality may be maintained by an ongoing process of activity-dependent plasticity. Here, we address this question in the context of rhythmogenesis. Specifically, we investigated the hypothesis that rhythmic activity in the brain can develop and be stabilized via activity-dependent plasticity in the form of spike-timing-dependent plasticity (STDP), thus extending our previous work that demonstrated rhythmogenesis in a toy model of two effective neurons. We examined STDP dynamics in large recurrent networks in two stages. We first derived the effective dynamics of the order parameters of the synaptic connectivity. Then, a perturbative approach was applied to investigate stability. We show that for a wide range of parameters, STDP can induce rhythmogenesis. Moreover, STDP can suppress synaptic fluctuations that disrupt functionality. Interestingly, STDP can channel fluctuations in the synaptic weights into a manifold in which the network activity is not affected, thus maintaining functionality while allowing a subspace in which synaptic weights can be widely distributed.