Neuronal development articles from across Nature Portfolio

Prenatal androgen excess disrupts cortical development and behavior primarily in male mice. Here, authors identify a non-canonical androgen receptor pathway in which AR cooperates with MeCP2 to regulate Mef2c and cortical neurogenesis.

Genetic variants can lead to variable outcomes in neurodevelopmental disorders. Here, the authors show that the 16p12.1 deletion and genetic background jointly shape chromatin regulation and neurodevelopmental phenotypes, explaining variable disease expressivity.

Somatostatin-positive interneurons exhibit peak neurite complexity during fetal and postnatal stages followed by pruning in adolescence and a peak in density during childhood, suggesting potential roles in critical periods of auditory plasticity.

Here authors generate a multi-omics atlas of the perinatal Bama miniature pig brain, revealing a conserved developmental inflection point marked by large-scale transcriptomic and proteomic shifts associated with synaptogenesis and gliogenesis.

The transcription factor ATF4 is shown to regulate double-stranded DNA repair within vulnerable CUX2⁺ upper-layer 2/3 cortical neurons, enabling their survival during development.

NeMO Analytics is a compendium of public transcriptomic data focused on the neocortex, enabling biologists without coding expertise to explore hundreds of datasets. Joint decomposition of these data yields insight into brain development and its modeling.

Two studies use single-nucleus multiomic sequencing to profile molecular and cellular dysfunction in the prenatal and early postnatal cortex in Down syndrome.

Neuronal activity drives parvalbumin-expressing interneuron maturation in the mouse cortex via its effects on the transcriptional cofactor PGC1α.

A study finds that microglia depletion has no effect on experience-dependent maturation of visual cortex circuitry in mice.

The centrosome is crucial for the microtubule dynamics that underlie the radial migration of developing rodent neurons but is not required for axon growth.

Preventing transient defects in postnatal cortical circuit function limits disease progression in a mouse model of Huntington disease.