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A general cytoplasmic signaling mechanism for the novel functions of diverse alpha protocadherins in cortical neuron migration and actin cytoskeletal dynamics as well as dendrite morphogenesis in the brain.

The flexible network architecture of the brain is sensitive to the modulation of neural gain, which may be mediated by ascending arousal nuclei, such as the noradrenergic locus coeruleus.

An evolutionarily conserved neuron-specific and stimulus-dependent enhancer region downstream of the Bdnf exon III regulates the expression of Bdnf transcripts starting from the upstream 5' exons.

RNA sequencing and conditional Nova mutants reveal that Nova protein function is necessary for activity-dependent alternative splicing of synaptic genes within somatostatin cortical interneurons and regulates its afferent and efferent connectivity.

Microtubules are nucleated by the centrosome of the primary cilium in the apical end-foot of neuroepithelial cells and inter-dependent microtubule and actin dynamics are required here to orchestrate delamination of newborn neurons.

In postnatal retina, neuronal apoptosis promotes a spectrum of microglial transcriptional states with varied dependence on CSF1R; TAM receptor Mer and complement receptor 3 mediate phagocytosis of dying neurons while altered CSF1R dependence requires Axl.

Neuronal interacting proteome reveals that the cellular dynamics of the lissencephaly-associated extracellular matrix receptor dystroglycan are governed by the exocyst complex, which is key for proper brain assembly.

Neurite geometry enables expansive and highly-branched neuronal structures to operate like single electrical compartments and simple linear integrators.

Extended biochemical and functional analyses in primary neurons show that early neuronal morphogenesis critically relies on cooperation of the actin nucleator Cobl and its ancestor Cobl-like and uncover their cooperative mechanisms at dendritic branch initiation sites.

The PRMT1 protein mediates arginine methylation of KCNQ2 channels to control neuronal excitability.