Joel C. Nicolau

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Mice lacking the Girk2 subunit of G protein-gated inwardly rectifying K+ (Girk) channels exhibit dopamine-dependent hyperactivity and elevated responses to drugs that stimulate dopamine neurotransmission. The dopamine-dependent phenotypes seen in Girk2(-/-) mice could reflect increased intrinsic excitability of or diminished inhibitory feedback to midbrain(More)
The stimulation of inhibitory neurotransmitter receptors, such as γ-aminobutyric acid type B (GABA(B) ) receptors, activates G protein-gated inwardly-rectifying K(+) (GIRK) channels, which influence membrane excitability. There is now evidence suggesting that G protein-coupled receptors and G protein-gated inwardly-rectifying K(+) [GIRK/family 3 of(More)
Voltage-gated sodium channels are responsible for action potential initiation and propagation in electrically excitable cells. In this study, we used biochemical, immunohistochemical and quantitative immunoelectron microscopy techniques to reveal the temporal and spatial expression of the Nav1.2 channel subunit in granule cells of cerebellum. Using(More)
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