Peripheral injury induces a programmed but reversible transformation of gene expression in somatosensory neurons providing a mechanism to regulate sensory input during wound healing.

Signals from different tactile submodalities are integrated optimally to culminate in cortical responses whose rate and timing conveys stimulus information.

A pain-relaying ion channel on a hypersensitive population of sensory neurons can instead elicit sensations of itch in both fish and mice when directly activated, providing a novel model of itch transduction.

Primary motor cortex afferents supra-linearly amplify the responses and sharpen angular tuning of neurons in the S1 barrel cortex.

Nonlinear elasticity of skin tissues and somatosensory neural responses are combined to predict and test C. elegans processing of touch stimuli and modifications due to changes in the body mechanics.

Understanding others' pain is grounded in cognitive rather than sensory faculties.

Constitutive sphingosine 1-phosphate signaling via the G-protein coupled receptor S1PR3 in mechanonociceptive somatosensory neurons is required for normal behavioral responses to noxious mechanical stimuli.

VIP-expressing cortical interneurons represent organism-level information about reward and punishment for local microcircuits to regulate local processing and plasticity.

Cross-modal stimuli are represented in the primary gustatory cortex according to their sensory identity, associability and predictive value.

Single neurons in human posterior parietal cortex encode actual and imagined touch within a shared neural substrate.