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Oxytocin neurons in the paraventricular nucleus of the hypothalamus mediate the increased sociability as a consequence of acute social isolation during adolescence via ventral tegmental area circuits.

Non-imprinted genes can contribute to parent-of-origin effects on phenotype through interactions with imprinted genes.

The transformation of multiple streams of sensory information into an estimate of body motion occurs between the cerebellum and deep cerebellar nucleus to ensure postural and perceptual stability.

The activity of cerebellar Purkinje cells both represents and participates in organizing the temporal structure of a periodically performed motor action.

A systematical study of pslG mutants at both a single cell and community level reveals the importance of intracellular glycosyl hydrolase PslG on the cell fate and biofilm development of P. aeruginosa, an opportunistic pathogen that can cause persistent infections.

A medaka mutant revealed that Wnt11 promotes formation of uniquely large protrusions from non-myogenic dorsal dermomyotome cells, which guide the epaxial myotome dorsally to achieve the coverage of the neural tube.

When human participants are able to plan responses in a visuo-spatial working memory task, sensory-like representations of remembered spatial position in early visual and parietal cortex adaptively trade off with motor-like representations of upcoming actions in sensorimotor cortex.

Wild-type human recombinant tau protein infused in presynaptic terminals newly assembled microtubules, which sequestered cytosolic dynamins, thereby blocking synaptic vesicle endocytosis and causing activity-dependent rundown of excitatory synaptic transmission in a slice model of mouse brainstem.

In postnatal retina, neuronal apoptosis promotes a spectrum of microglial transcriptional states with varied dependence on CSF1R; TAM receptor Mer and complement receptor 3 mediate phagocytosis of dying neurons while altered CSF1R dependence requires Axl.

This first evidence of oligogenic inheritance in failed spermatogenesis strongly suggests that oligogenic heterozygosity could explain a significant proportion of asthenoteratozoospermia cases.