Browse our latest Neuroscience articles

Transient suppression of activity in the macaque mediodorsal thalamus impairs adjustment of secondary reinforcer values and disrupts appropriate action selection in a reinforcer devaluation task; this profile is distinct from that of amygdala or subregions of orbitofrontal cortex.

In vivo and ex vivo analysis of the activity-regulated gene Rem2 in the mouse visual system sheds new light on the contribution of intrinsic excitability in circuit plasticity.

The numerous reports in support of action-value representation in the striatum are based on statistical analyses that are subject to two critical confounds and, thus, this long-held belief of striatal action-value representation should be retested using different experiments and analyses.

A dynamic SILAC analysis reveals that neuronal proteome turnover is influenced by the cell type as well as the extracellular environment.

Developmental hearing loss causes perceptual deficits that are best explained by degraded auditory cortical encoding that is recorded during task performance.

Multiple independent directional selection events on a neural substrate that underpins domain-general associative abilities partly explains independent occurrences of complex behavior in different lineages of mammals.

Molecular labeling, electrophysiology and calcium imaging have revealed a novel switching of neurotransmitter at the frog neuromuscular junction where motoneurons transiently release glutamate before acetylcholine at synapses on developing hindlimb muscles at the onset of metamorphosis.

The technique of serial blockface scanning electron microscopy, which permits the complete reconstruction of neuronal structures, allows comparison of the detailed "wiring diagrams" of lateral-line receptor organs in wild-type and mutant zebrafish.

Social-interaction impairment in germ-free mice is associated with a markedly altered transcriptional response to social novelty in the amygdala, as characterised by replacement of upregulation of common stimulus-induced pathways with upregulation of the splicing machinery.

Loss of a developmentally essential gene in adulthood is tolerated in mice, thus offering potential therapeutic options for Alzheimer's and Parkinson's disease.