Frontal cortical circuit alterations and cognitive deficits identified in mouse genetic models are reversed by chemogenetic or optogenetic stimulation of the mesocortical dopamine circuit in an adolescent period.

A subset of genes in the mouse brain show dynamically regulated and unequal expression of maternally and paternally derived variants, with implications for brain development and function.

Intersectional genetics show that excitatory neurons are essential for the functional and anatomical maturation of cerebellar circuits in mice.

Munc13 proteins are key determinants of large dense-core vesicle (LDCV)-dependent catecholamine release in chromaffin cells.

Impairing TDP-43 RNA-binding capacity through a single acetylation-mimic mutation alters TDP-43 function and recapitulates biochemical, molecular, and behavioral features of sporadic TDP-43 proteinopathies, thus providing opportunities for new research into pathogenic mechanisms and therapeutic interventions.

A single amino acid change in a neuronal ion channel called KCNQ2 blocks ion flow, prevents protein localization on axons, and results in severe epilepsy and slowed neurological development.

Analysis of AnkyrinR conditional knockout mice shows that AnkyrinR regulates PV+ fast-spiking interneurons by organizing and maintaining perineuronal nets and through the membrane clustering of Kv3.1b K⁺ channels.

The messenger RNA encoding La-related protein-4 (LARP4) contains a short region of instability whose codon clusters are sensitive to low abundance tRNAs that when elevated increase LARP4 activity for poly(A) lengthening of ribosomal protein mRNAs and other mRNAs.

COPII vesicles regulate the metabolism of cholesterol through the selective transport of secretory proteins.