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Sodium currents in vagotomized primary afferent neurones of the rat

Eric Lancaster * and Daniel Weinreich *†

1. 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 µM 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.

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