GluN2B-NMDAR Allosteric modulator 1

The Open Field Test is a rodent behavioral assay that measures spontaneous locomotion, exploratory behavior, and anxiety-like behavior when an animal is placed in a novel open arena. The main readouts are total distance traveled, movement time, velocity, center-zone entries, center-zone time, peripheral-zone time, and thigmotaxis. The assay is based on the conflict between exploration of a novel environment and avoidance of exposed open areas; higher center exploration is commonly interpreted as lower anxiety-like behavior, whereas increased wall-following or peripheral occupancy is interpreted as higher anxiety-like behavior.

The Elevated Plus Maze is a rodent anxiety-like behavior assay based on the conflict between spontaneous exploration and avoidance of open, elevated, exposed spaces. The apparatus contains two open arms and two closed arms arranged in a plus shape, and rodents normally spend more time in closed arms than open arms. The assay readout is generated by recording arm entries, time spent in open and closed arms, and related exploratory behaviors. Increased open-arm time or open-arm entries is commonly interpreted as reduced anxiety-like behavior, whereas reduced open-arm exploration is interpreted as increased anxiety-like behavior.

PINK1/Parkin-mediated mitophagy pathway is a mitochondrial quality-control signaling axis in which mitochondrial depolarization stabilizes PINK1 on damaged mitochondria, activates Parkin recruitment and E3 ubiquitin ligase activity, promotes ubiquitination of outer mitochondrial membrane proteins, recruits selective autophagy adaptors, and drives lysosomal degradation of damaged mitochondria. In neurological disease research, this pathway is experimentally important because neurons, especially dopaminergic neurons, are highly dependent on mitochondrial integrity, and defective mitochondrial turnover can lead to mitochondrial dysfunction, oxidative stress, impaired neuronal survival, α-synuclein accumulation, and neuroinflammatory damage-associated signals. The genetic disease link is strongest in Parkinson’s disease because mutations in PRKN/parkin cause autosomal recessive juvenile parkinsonism, mutations in PINK1 cause hereditary early-onset Parkinson’s disease, and Drosophila studie