The transcription factor Pou3f1 triggers embryonic stem cells to become neuronal progenitor cells in two ways: by activating the expression of pro-neuronal genes and by blocking external inhibitory signaling cascades.
Retinal waves are correlated with calcium transients in Müller cells, demonstrating that spontaneous activity encompasses both neuronal and glial networks during a crucial period of retinal development.
Closure of the cranial neural tube, which is essential for mammalian development, is driven by spatially and temporally patterned cell remodeling events that require positionally regulated Sonic hedgehog signaling.
An unbiased genetic screen in Drosophila provides evidence for a direct link between glial Ca2+ 25 signaling and classical functions of glia in buffering external K+ as a mechanism to regulate neuronal excitability.
Placing the PACAP/PAC1 signaling within glutamate/GABA cell type and subregional contexts in mouse brain reveals its conspicuous role for sensorimotor circuit interaction through modulating neuronal plasticity.
Chronic engagement of Natural killer cell inhibitory receptors by MHC-I molecules maintains a high activity of the mTOR pathway allowing subsequent amplification of signaling through activating receptors upon acute stimulation.