Natalia Gorelova

TL;DR: D1 and D2 receptors regulated GABAergic activity in opposite manners and through different mechanisms in prefrontal cortex (PFC) pyramidal cells, which could have important implications for the computational properties of active PFC networks.

TL;DR: This whole cell patch-clamp study shows that DA induced a direct, TTX-insensitive, reversible membrane depolarization, and increased the excitability of fast-spiking (FS) interneurons, which could represent a mechanism via which DA suppresses persistent firing of pyramidal neurons in vivo.

TL;DR: These electrophysiological and morphological properties of the four principal pyramidal PFC cell types have provided valuable details for understanding further how PFC processes input and transmit outputs to regions such as the NAc.

TL;DR: It is hypothesized that the dysfunctional mesocortical dopamine input to the PFC may lead to abnormal modulation of ionic channels distributed in the dendritic–somatic compartments of PFC pyramidal neurons that project to the ventral tegmental area and/or nucleus accumbens.

TL;DR: It is proposed that a D1/D5 agonist-induced leftward shift in the activation of I(NaP) enables DA to facilitate the firing of PFC neurons in response to depolarizing inputs.