Altered activity of ATP-sensitive K⁺ channels underlies the metabolic seizure resistance produced by genetic manipulation of the BAD protein in mice.

LARP1 turns off and on the translation of an essential class of mRNAs by acting as a key effecter and regulator for mTORC1.

The cellular and molecular substrates that underlie the programmed behavioral response to a gustatory sex pheromone have been identified.

Lovastatin ability to rescue motor deficits and survival in a mouse model of Rett syndrome is strongly influenced by the genetic background.

Seizures stimulate estrogen synthesis in the brain and acutely inhibiting brain estrogen synthesis suppresses seizures, in both sexes, without additional interventions.

Vanishing White Matter Disease mutations compromise the function of the essential translation initiation factor eIF2B by destabilizing the holoenzyme, and the small molecule ISRIB reverses their pathogenic effect by promoting complex formation.

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

Oligodendrocytes in white matter use Kir4.1 inwardly rectifying potassium channels to prevent extracellular potassium accumulation, enabling neurons to sustain repetitive firing and limiting the initiation of seizures.

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.

Improved two-photon fluorescence microendoscopy enables volumetric imaging of synapses and neurons in deep brain structures in vivo.