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Properties of sodium currents in neonatal and young adult mouse superficial dorsal horn neurons
- 作者:Melissa A Tadros ; Kristen E Farrell ; Brett A Graham ; Alan M Brichta…
- 关键词:Development ; Activation ; Spinal cord ; Pain ; Action potential
- 刊名:Molecular Pain
- 出版年:2015
- 出版时间:December 2015
- 年:2015
- 卷:11
- 期:1
- 全文大小:5,490 KB
- 参考文献:1. Walsh, MA, Graham, BA, Brichta, AM, Callister, RJ (2009) Evidence for a critical period in the development of excitability and potassium currents in mouse lumbar superficial dorsal horn neurons. J Neurophysiol 101: pp. 1800-12 external" href="http://dx.doi.org/10.1152/jn.90755.2008" target="_blank" title="It opens in new window">CrossRef
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- 出版者:BioMed Central
- ISSN:1744-8069
文摘
Background Superficial 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. Results Whole 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 ?00?mV. Poorly clamped currents, based on a deflection in the IV relationship at potentials between ?0 and ?0?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. Conclusions Our 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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