• Melissa A Tadros, Kristen E Farrell, Brett A Graham, Alan M Brichta, and Robert J Callister.
• School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine and Hunter Medical Research Institute, The University of Newcastle, Callaghan, Newcastle, NSW, 2308, Australia. melissa.tadros@newcastle.edu.au.
• Mol Pain. 2015 Jan 1;11:17.

BackgroundSuperficial dorsal horn (SDH) neurons process nociceptive information and their excitability is partly determined by the properties of voltage-gated sodium channels. Recently, we showed the excitability and action potential properties of mouse SDH neurons change markedly during early postnatal development. Here we compare sodium currents generated in neonate (P0-5) and young adult (≥P21) SDH neurons.ResultsWhole cell recordings were obtained from lumbar SDH neurons in transverse spinal cord slices (CsF internal, 32°C). Fast activating and inactivating TTX-sensitive inward currents were evoked by depolarization from a holding potential of -100 mV. Poorly clamped currents, based on a deflection in the IV relationship at potentials between -60 and -50 mV, were not accepted for analysis. Current density and decay time increased significantly between the first and third weeks of postnatal development, whereas time to peak was similar at both ages. This was accompanied by more subtle changes in activation range and steady state inactivation. Recovery from inactivation was slower and TTX-sensitivity was reduced in young adult neurons.ConclusionsOur study suggests sodium channel expression changes markedly during early postnatal development in mouse SDH neurons. The methods employed in this study can now be applied to future investigations of spinal cord sodium channel plasticity in murine pain models.

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