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Julie Dethier

Publications and source records attributed to Julie Dethier.

2 recordsLinked to original sources

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

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.

q-bio.NC

Modulation of beta oscillations during movement initiation: modeling the ionic basis of a functional switch

We use a computational model to propose a physiological mechanism by which transient control of beta oscillations in the indirect pathway of the basal ganglia is orchestrated at the cellular level. Our model includes a simple and robust mechanism by which a cellular switch (from bursting to tonic) almost instantaneously translates into a functional gating switch (from blocking to conducive) in an excitatory-inhibitory network. Applied to the control of beta oscillations in the basal ganglia, the model shows the modulation of beta activity under the action of a transient depolarization, for instance a dopamine signal. The model predicts, by analogy to the thalamocortical circuit, a novel gating function by which the transfer of cortical spikes through the indirect pathway is blocked under the inhibitory drive preceding movement but briefly released at the onset of movement execution.

q-bio.NC