Contributions of Nociresponsive Area 3a to Normal and Abnormal Somatosensory Perception

Traditionally, cytoarchitectonic area 3a of primary somatosensory cortex (SI) has been regarded as a proprioceptive relay to motor cortex. However, neuronal spike-train recordings and optical intrinsic signal imaging, obtained from nonhuman sensorimotor cortex, show that neuronal activity in some of the cortical columns in area 3a can be readily triggered by a C-nociceptor afferent drive. These findings indicate that area 3a is a critical link in cerebral cortical encoding of secondary/slow pain. Also, area 3a contributes to abnormal pain processing in the presence of activity-dependent reversal of gamma-aminobutyric acid A receptor-mediated inhibition. Accordingly, abnormal processing within area 3a may contribute mechanistically to generation of clinical pain conditions. PERSPECTIVE: Optical imaging and neurophysiological mapping of area 3a of SI has revealed substantial driving from unmyelinated cutaneous nociceptors, complementing input to areas 3b and 1 of SI from myelinated nociceptors and non-nociceptors. These and related findings force a reconsideration of mechanisms for SI processing of pain.