Browse our latest Neuroscience articles

Gustatory information and hunger state impinge on a local, multilayered circuit that drives feeding initiation.

A theoretical model combines self-supervised predictive learning with structural inductive biases to reveal how quasi-continuous attractors that perform accurate angular path integration can be learned from experience during development in the Drosophila and potentially other animal models.

A combination of physiological, histological, and optical approaches reveals synapse-specific function of α-synuclein in mouse brain under both normal and pathological states.

Prelimbic cortical inputs are differentially recruited during early memory consolidation, with claustrum projections involved at encoding and insular cortex projections recruited for recent recall.

The brain’s projection of linguistic knowledge onto speech is reflected by the automatic, reflexive neural tracking of phrases, while the distribution of phrasal-rate tracking and connectivity, particularly the involvement of inferior frontal cortex, is subject to task demands.

Electrophysiological and genetic analyses reveal a biophysical mechanism in parvalbumin interneurons, uncoupled from changes in gene expression, resulting in reduced cortical inhibition in early-stage Alzheimer's disease.

Hypothalamic stress effector neurons rapidly change activity patterns via recurrent inhibition, representing state-dependent activity switch between baseline and elevated stress levels.

By acting as versatile signal-processors that encode flexible coordinate representations, muscle spindles challenge current widely held views concerning the role of proprioceptors and the peripheral nervous system in sensorimotor function.

The majority of hippocampal neurons in CA3 experience inhibition before and during ripple buildup, while dentate and CA1 cells display depolarizing transients preceding and following ripple onset pointing to a long and orchestrated awake ripple initiation process.

Among three new models for KCNMA1 channelopathy, the most severe gain-of-function variant (Kcnma1^N999S/WT) displays a particular type of immobilizing paroxysmal dyskinesia observed in patients, including amphetamine responsiveness.