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.
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.
A class of interneuron is identified that promotes escape behavior downstream of nociceptor inputs via connections to nociceptive integrator and premotor networks.
The Drosophila equivalent of Substance P signaling modulates nociceptive sensitization by regulating Hedgehog signaling within nociceptive sensory neurons.
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.
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.
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.
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.
Pro-nociceptive and pro-inflammatory TRPM3 (transient receptor potential melastatin 3) channels, expressed in somatosensory neurons, are inhibited by activation of Gαi-coupled receptors, such as µ-opioid receptors, in vitro and in vivo.
