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  • 1
    Nodose ganglion neurones (NGNs) become less excitable following section of the vagus nerve. To determine the role of sodium currents (INa) in these changes, standard patch-clamp recording techniques were used to measure INa in rat NGNs maintained in vivo for 5–6 days following vagotomy, and then in vitro for 2–9 h.
  • 2
    Total INa and INa density in vagotomized NGNs were similar to control values. However, steady-state INa inactivation in vagotomized NGNs was shifted −9 mV relative to control values (V11/2sol;2, −74 ± 2 vs.−65 ± 2 mV, P < 0.01) and INa activation was shifted by −7 mV (V11/2sol;2, −21 ± 2 vs.−14 ± 2 mV, P < 0.006). INa recovery from inactivation was also slower in vagotomized NGNs (fast time constant, 2.8 ± 0.4 vs. 1.6 ± 0.3 ms, P < 0.02).
  • 3
    The fraction of INa resistant to 1 μm tetrodotoxin (TTX-R) was halved in vagotomized NGNs (21 ± 8 vs. 56 ± 8 % of total INa, P < 0.05). This change from TTX-R INa to TTX-sensitive (TTX-S) INa may explain altered INa activation, inactivation and repriming in vagotomized NGNs.
  • 4
    The contribution of alterations in INa to NGN firing patterns was assessed by measuring INa evoked by a series of action potential (AP) waveforms. In general, control NGNs produced large, repetitive TTX-R INa while vagotomized NGNs produced smaller TTX-S INa that rapidly inactivated during AP discharge. We conclude that TTX-R INa is important for sustained AP discharge in NGNs, and that its diminution underlies the decreased AP discharge of vagotomized NGNs.