Abstract

In humans converging evidence indicates that affective aspects of touch are signaled by low threshold mechanoreceptive C tactile (CT) afferents. Analyses of electrophysiological recordings, psychophysical studies in denervated subjects, and functional brain imaging, all indicate that CT primary afferents contribute to pleasant touch and provide an important sensory underpinning of social behavior. Considering both these pleasant and social aspects of gentle skin-to-skin contact, we have put forward a framework within which to consider CT afferent coding properties and pathways—the CT affective touch hypothesis. Recent evidence from studies in mice suggests that CTs, when activated, may have analgesic or anxiolytic effects. However, in neuropathic pain conditions, light touch can elicit unpleasant sensations, so called tactile allodynia. In humans, tactile allodynia is associated with reduced CT mediated hedonic touch processing suggesting loss of the normally analgesic effect of CT signaling. We thus propose that the contribution of CT afferents to tactile allodynia is mainly through a loss of their normally pain inhibiting role.

Highlights

  • Human tactile sensibility was considered to be mediated solely by low-threshold mechanoreceptors with large myelinated (Aβ) afferents conducting impulses at high speed

  • IN SUBJECTS LACKING C AFFERENTS We have examined patients with a hereditary disorder associated with a nerve growth factor beta (NGFB) gene mutation causing a denervation pattern opposite to that of the neuronopathy subjects GL and IW

  • Carriers of the NGFB mutation show a reduction in density of thinly myelinated and unmyelinated nerve fibers, likely including C TACTILE (CT) afferents, whereas their Aβ afferents are intact

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Summary

Introduction

Human tactile sensibility was considered to be mediated solely by low-threshold mechanoreceptors with large myelinated (Aβ) afferents conducting impulses at high speed (around 50 m s−1). The dependency on Aβ signaling was largely based on nerve block experiments in healthy subjects demonstrating a lack of tactile sensations when Aβ fibers were blocked through pressure applied on the nerve (Mackenzie et al, 1975).

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