Somatosensory Cortical Signature of Facial Nociception and Vibrotactile Touch Induced Analgesia

Abstract

Pain relief by vibrotactile touch is a common human experience. Previous neurophysiological investigations in animals focused on spinal mechanisms while human studies suggested the involvement of supraspinal mechanisms. Here we asked whether and how the primary somatosensory cortex (S1) is involved in touch induced analgesia. We discovered that in mice, vibrotactile reafferent signals from self-generated whisking significantly reduce facial nociception, which is abolished by specifically blocking touch transmission from thalamus to the barrel cortex (S1B). The presence of whisking altered nociceptive signal processing in S1B neurons. Intrinsic manifold analysis of S1B population activity revealed that whisking pushes the transition of neural state induced by noxious stimuli towards the state encoding non-nocifensive actions. Thus, S1B integrates facial tactile and noxious signals to enable touch mediated analgesia. TeaserVibrotactile signals modulate barrel cortex population dynamics during touch mediated facial analgesia