Drosophila polymodal nociceptors use precipitous fluctuation of the firing rate, which depends on Ca²⁺ influx, as a key signal encoding a heat sensation and evoking the robust heat avoidance behavior.

Drosophila nociceptive neurons convert high-intensity stimuli into characteristic fluctuations of firing rates, quiescent periods of which are regulated by hyperpolarization through small conductance Ca²⁺-activated K⁺ channels.

Electrophysiological experiments, Ca²⁺ imaging, and behavioral studies in mice identify the TRPM3 ion channel as a novel target of G-protein βγ subunits.

Chronic pain distorts intensity coding in the anterior cingulate cortex to give rise to generalized anatomically nonspecific enhancement in pain aversion.

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.

Epidermal cells in vertebrates and invertebrates ensheath portions of somatosensory neurons via a conserved morphogenetic mechanism, and this ensheathment regulates morphogenesis and function of Drosophila nociceptive neurons.

Greater connectivity of the descending pain modulatory system network in the infant brain is associated with lower pain-related brain activity.

Optogenetics reveals that keratinocytes can evoke action potential firing in several types of cutaneous sensory afferents, including those that transmit thermal, mechanical and pain stimuli.

A class of interneuron is identified that promotes escape behavior downstream of nociceptor inputs via connections to nociceptive integrator and premotor networks.

Keratinocytes are critical for normal innocuous and noxious touch through their mechanically evoked ATP release and subsequent signaling to P2X4 channels on sensory neurons.