Peripheral inflammation increases the functional coherency of spinal responses to tactile but not nociceptive stimulation.

Abstract

Reorganization of central networks and plasticity of neuronal representations have been implicated in recent years in the dynamic expression of somatosensory responses. The functional properties of spinal cells were shown to change in the scale of minutes after peripheral high-intensity stimulations and to undergo profound alterations in their responses in experimental models of chronic pain. These observations, however, are restricted to recordings from individual cells, and no information exists on how these changes may be reflected on the activity of somatosensory neuronal networks involved in pain processing. To understand how spinal cord networks may be altered after the onset of hyperalgesia, we extracellularly recorded from groups of five to nine neighboring neurons in the hindlimb representation area of the dorsal horn. The multineuronal activity evoked by cutaneous innocuous and noxious stimulation was compared before and for 3 h after the subcutaneous injection of diluted formalin. Formalin caused immediate changes in response properties and mechanical threshold of activation for the majority of the neurons and induced the incorporation of previously unresponsive neighboring neurons to the functional network. Analysis of the temporal correlation within the neuronal population revealed that formalin-induced inflammation increased the functional coherence of the network to the nonnociceptive stimulation but not to the painful stimuli. This increase in the tactile acuity of populations of nociceptive neurons may be a basis for the emergence of touch-evoked pain.