Carmen C. Canavier

The paper models midbrain dopamine neuron subpopulations to show how slow dynamics enhance robustness of regular pacemaking against noise.

The paper investigates how excitation and inhibition shape theta-gamma coupling in the medial entorhinal cortex using experimental and computational methods, revealing distinct cell-type contributions to oscillatory activity.

The paper uses nullcline analysis to explain how differences in electrical activity between subpopulations of midbrain dopamine neurons arise from variations in Kv4 channel dynamics and AHP strength.

The paper shows fast-spiking interneurons sustain gamma oscillations via ING mechanisms, with excitation strength tuning the oscillatory regime between ING and PING.

This paper develops a mean field theory for pulse-coupled oscillators using phase response curves to predict network synchronization stability and frequency.

The paper investigates the biophysical and mathematical mechanisms of persistent firing interruption in parvalbumin-expressing interneurons, showing how Kv1 channel inactivation enables robust persistent silencing.

The paper compares the robustness of gamma oscillations in inhibitory networks with hyperpolarizing versus shunting inhibition, showing hyperpolarizing inhibition enhances synchrony robustness to noise.

The paper updates stability criteria for synchrony in pulse-coupled oscillator networks to include conduction delays and shows how alternating firing patterns can enforce cluster synchrony.

The paper identifies TRPM4 channels as key mediators of cholinergic modulation of firing rate adaptation in CA1 pyramidal neurons during depolarizing ramps.

The paper models interneuronal networks in the medial entorhinal cortex to show how hyperpolarizing and shunting inhibition affect theta-nested fast oscillations through gap junctions and synaptic depression.

The paper identifies KChIP4a as a biophysical regulator that selectively affects inhibitory integration and learning in dopamine neurons projecting to the nucleus accumbens core.

The paper investigates how long-term inactivation of NaV1.6 sodium channels contributes to adaptation in CA1 pyramidal neurons through a combined experimental and computational approach.

This study examines how type 1 and type 2 excitability in inhibitory interneurons affects synchronization and modulation in neural networks under different inhibitory conditions.