A positive feedback at the cellular level promotes robustness and modulation at the circuit level

TL;DR

This paper demonstrates that a slow-positive feedback mechanism at the cellular level, specifically via T-type calcium currents, enhances the robustness and modulation of rhythmic circuits like half-center oscillators.

Contribution

It reveals that slow-positive feedback from T-type calcium currents is essential for the robustness and modulation of rhythmic neural circuits, advancing understanding of cellular contributions to circuit dynamics.

Findings

Slow-positive feedback via T-type calcium currents is necessary for rhythmic robustness.

The presence of this feedback enables physiological modulation of the circuit.

The study identifies a cellular property crucial for network modeling of robustness.

Abstract

The paper highlights the role of a positive feedback gating mechanism at the cellular level in the robust- ness and modulation properties of rhythmic activities at the circuit level. The results are presented in the context of half-center oscillators, which are simple rhythmic circuits composed of two reciprocally connected inhibitory neuronal populations. Specifically, we focus on rhythms that rely on a particu- lar excitability property, the post-inhibitory rebound, an intrinsic cellular property that elicits transient membrane depolarization when released from hyperpolarization. Two distinct ionic currents can evoke this transient depolarization: a hyperpolarization-activated cation current and a low-threshold T-type calcium current. The presence of a slow activation is specific to the T-type calcium current and provides a slow-positive feedback at the cellular level that is absent in the cation current. We show that this slow- positive feedback is necessary and sufficient to endow the network rhythm with physiological modulation and robustness properties. This study thereby identifies an essential cellular property to be retained at the network level in modeling network robustness and modulation.