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This Article Full Text Full Text (PDF) All Versions of this Article: 99/2/617    most recent 00944.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Pinto, V. Articles by Safronov, B. V. Search for Related Content PubMed PubMed Citation Articles by Pinto, V. Articles by Safronov, B. V.

Role of TTX-Sensitive and TTX-Resistant Sodium Channels in A- and C-Fiber Conduction and Synaptic Transmission

¹Instituto de Biologia Molecular e Celular, Universidade do Porto, Porto, Portugal; ²Laboratório de Biologia Celular e Molecular, Faculdade de Medicina, Universidade do Porto, Porto, Portugal; and ³Vollum Institute, Oregon Health and Science University, Portland, Oregon

Submitted 21 August 2007; accepted in final form 2 December 2007

Thin afferent axons conduct nociceptive signals from the periphery to the spinal cord. Their somata express two classes of Na⁺ channels, TTX-sensitive (TTX-S) and TTX-resistant (TTX-R), but their relative contribution to axonal conduction and synaptic transmission is not well understood. We studied this contribution by comparing effects of nanomolar TTX concentrations on currents associated with compound action potentials in the peripheral and central branches of A- and C-fiber axons as well as on the A- and C-fiber-mediated excitatory postsynaptic currents (EPSCs) in spinal dorsal horn neurons of rat. At room temperature, TTX completely blocked A-fibers (IC₅₀, 5–7 nM) in dorsal roots (central branch) and spinal, sciatic, and sural nerves (peripheral branch). The C-fiber responses were blocked by 85–89% in the peripheral branch and by 65–66% in dorsal roots (IC₅₀, 14–33 nM) with simultaneous threefold reduction in their conduction velocity. At physiological temperature, the degree of TTX block in dorsal roots increased to 93%. The A- and C-fiber-mediated EPSCs in dorsal horn neurons were also sensitive to TTX. At room temperature, 30 nM blocked completely A-input and 84% of the C-fiber input, which was completely suppressed at 300 nM TTX. We conclude that in mammals, the TTX-S Na⁺ channels dominate conduction in all thin primary afferents. It is the only type of functional Na⁺ channel in A-fibers. In C-fibers, the TTX-S Na⁺ channels determine the physiological conduction velocity and control synaptic transmission. TTX-R Na⁺ channels could not provide propagation of full-amplitude spikes able to trigger synaptic release in the spinal cord.

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