A Short Report
نویسنده
چکیده
Single-unit recordings from monkey spinothalamic tract (STT) neurons reveal that the responses of polymodal nociceptive lamina I STT neurons correspond with the profile of burning pain elicited in human subjects by repeated brief-contact heat. In contrast, lamina V wide-dynamicrange (WDR) neurons show a significantly different response pattern. This finding indicates that burning pain is signaled by modality-selective lamina I neurons, not convergent lamina V WDR neurons. INTRODUCTION The issue of specificity and integration in the neural representation of pain has been fervently debated for over a century. At present, the critical role of the spinothalamic tract (STT) in pain is universally acknowledged, but the relative contributions to pain sensation of modalityselective lamina I nociceptive neurons and convergent “wide-dynamic-range” (WDR) lamina V neurons are controversial (Craig 2003; Price et al. 2003). Proponents of the widely held pattern / intensity concept of pain sensation profess that WDR lamina V STT neurons (the “pain transmission” cells of gate control theory; Wall 1973) are “necessary and sufficient” for all types of pain sensation and that their discharge “encodes” pain (Willis and Westlund 1998; Price et al. 2003). Notably, even investigators who recognize a critical role for substance P-responsive lamina I neurons suppose that they contribute to pain sensation by modulating the activity of WDR lamina V STT cells (Khasabov et al. 2002; Hunt and Mantyh 2001). However, the evidence supporting a role of WDR lamina V cells in pain sensation is tenuous, and there are numerous fundamental incongruities (Craig 2003). The most obvious is the inherent modality-ambiguity of lamina V WDR cells. Whether considered singly or as a population, their intensity-related discharge cannot differentiate stimulus modality or tissue of origin, whereas human sensation certainly does both (Lewis 1942; Perl 1984; Carstens 1997; Craig 2003). In contrast, evidence in cats indicates that the activity of nociceptive-specific (NS) lamina I STT cells, dominated by A∗-fiber input, and polymodal nociceptive (HPC, for heat, pinch, and cold) lamina I STT cells, dominated by C-fiber input, can differentially signal the
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