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