synaptic conversion of chloride-dependent synapses in spinal nociceptive circuits roles in neuropathic painchloride-dependent突触的突触转换在神经性疼痛的脊椎疼痛的电路的角色.pdfVIP

Hindawi Publishing Corporation Pain Research and Treatment Volume 2011, Article ID 738645, 12 pages doi:10.1155/2011/738645 Research Article Synaptic Conversion of Chloride-Dependent Synapses in Spinal Nociceptive Circuits: Roles in Neuropathic Pain Mark S. Cooper and Adam S. Przebinda Department of Biology, University of Washington, Seattle, WA 98195-1800, USA Correspondence should be addressed to Mark S. Cooper, mscooper@ Received 25 December 2010; Accepted 21 March 2011 Academic Editor: Fani L. Neto Copyright © 2011 M. S. Cooper and A. S. Przebinda. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Electrophysiological conversion of chloride-dependent synapses from inhibitory to excitatory function, as a result of aberrant neuronal chloride homeostasis, is a known mechanism for the genesis of neuropathic pain. This paper examines theoretically how this type of synaptic conversion can disrupt circuit logic in spinal nociceptive circuits. First, a mathematical scaling factor is developed to represent local aberration in chloride electrochemical driving potential. Using this mathematical scaling factor, electrophysiological symbols are developed to represent the magnitude of synaptic conversion within nociceptive circuits. When inserted into a nociceptive circuit diagram, these symbols assist in understanding the generation of neuropathic pain associated with the collapse of transmembrane chloride gradients. A more generalized scaling factor is also derived to represent the interplay of chloride and bicarbonate driving potentials on the function of GABAergic and glycinergic synapses. These mathemat