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Diverse morphologies of Drosophila T4/T5 neuronal subtypes are defined by the modular assembly of transcriptional programs for distinct wiring features.

The shutoff of aerobic glycolysis in neuronal differentiation is essential for neuronal survival.

Genetic manipulations reveal how the spatiotemporal expression pattern of two RNA-binding proteins regulates the eventual number of motoneurons in a Drosophila neuronal lineage.

An interaction between the ion channel ASIC1a and the protein RIP1 is responsible for neuronal death caused by tissue acidosis.

While tau and aging have highly overlapping differential gene expression signatures, they diverge in the affected cell types, with aging having a wide-ranging impact and tau-triggered changes instead polarized to excitatory neurons and glia.

VGF was identified as a factor secreted from thalamocortical axons essential for the cytoarchitectonic features of neocortical layer 4 in the sensory areas in mice.

Control of neural stem cells by reactive oxygen species (ROS) provides a link between systemic shifts in oxygen tension and neuronal regeneration, and suggests an evolutionary driving force for the inherent ability of newts to regenerate their brain cells.

Novel transgenic zebrafish lines allow selective ablation of neuronal mitochondria by far red light, providing a powerful tool for investigating mitochondrial homeostasis in neurons and mitochondrial mechanisms in neurological disease.

Neuronal loss can be studied by passing electrical current through the same electrodes used for neuron measurement without disrupting recording ability.

The transcriptional cofactor HPK-1 (homeodomain-interacting protein kinase) functions as a key regulator of multiple proteostatic stress responses, each originating from discrete neuronal subtypes within the Caenorhabditis elegans nervous system to preserve neuronal health and maintain organismal proteostasis during normal aging.