Salvador Dura-Bernal, Benjamin A Suter ... William W Lytton
The NetPyNE software tool provides a framework to efficiently develop, simulate, optimize and analyze experimentally grounded neural models spanning the molecular, cellular and circuit scales.
The important role of serine biosynthesis in Müller cells may explain why the macula is so much more prone to developing disease than the rest of the retina.
Action-selection under response-conflict is buttressed by an inhibitory control signal from the basal ganglia that non-selectively suppresses motor excitability.
An effective and reversible mouse glaucoma model that replicates the secondary glaucoma in human patients caused by silicone oil after retina surgeries presents significant neurodegeneration, and is suitable for neuroprotectants selection.
Kevin Dorgans, Valérie Demais ... Frédéric Doussau
Molecular, structural and functional diversity of cerebellar granule cell inputs on single molecular layer interneurons extends information processing in feed-forward inhibition microcircuits.
Frederick Verbruggen, Adam R Aron ... C Nico Boehler
Clear guidelines and open-source software resources are provided for the stop-signal task, in order to streamline the use of this important tool, and to thereby increase its validity and reliability.
Early-generated interneurons are more mature in intrinsic properties and neuronal connectivity during early postnatal stage, and are critical for proper spontaneous network synchronization and the wiring of immature cortical circuits.
Even when the primary visual cortical area is absent bilaterally from early life, the rest of a primate visual brain can develop and function normally to support day-to-day visual behaviour.
Caesar M Hernandez, Caitlin A Orsini ... Jennifer L Bizon
Optogenetic approaches in young and aged rats define multiple roles for basolateral amygdala in guiding intertemporal choice, and show that these roles change across the lifespan.
Polyglutamine expansion in mutant huntingtin disrupts a novel transcription-coupled DNA repair complex, providing an undescribed mechanism of neuronal toxicity and degeneration in Huntington's disease.
