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

The extrinsic cue NGF and the intrinsic signal Islet1 converge at the level of the Runx1/CBFβ transcription factor complex formation to promote differentiation of a major nociceptor subtype.

The subthalamic nucleus is linked to a nociceptive network and involved in nociceptive processing and perception.

The Drosophila equivalent of Substance P signaling modulates nociceptive sensitization by regulating Hedgehog signaling within nociceptive sensory neurons.

A novel mechanism for gating nociceptive sensory-motor behavior is identified in freely behaving rats using high-speed videography that is controlled by posture and modulated by opioid and non-opioid receptor-dependent processes.

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.

MRGPRD and MRGRPX1 are co-expressed in primate DRG neurons, but β-alanine and BAM8-22, preferentially activate CMH-subclasses, and co-activating different cutaneous nociceptors by pruritogens does not change itch sensation to pain.

The mTOR downstream effector eukaryotic initiation factor 4E-binding protein 1 (4E-BP1) regulates mechanical nociception via translational control of synaptic transmission in the spinal cord.

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.

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.