Vagotomy decreases excitability in primary vagal afferent somata

Standard patch-clamp and intracellular recording techniques were used to mo nitor membrane excitability changes in adult inferior vagal ganglion neuron s (nodose ganglion neurons, NGNs) 5 days following section of the vagus ner ve (vagotomy). NGNs were maintained in vivo for 5 days following vagotomy, and then in vitro for 2-9 h prior to recording. Vagotomy increased action p otential (AP) threshold by over 200% (264 +/- 19 pA, mean +/- SE, = 66) com pared with control values (81 +/- 20 pA, n = 68; P < 0.001). The number of APs evoked by a 3 times threshold 750-ms depolarizing current decreased by >70% (from 8.3 to 2.3 APs, P < 0.001) and the number of APs evoked by a sta ndardized series of (0.1-0.9 nA, 750 ms) depolarizing current steps decreas ed by over 80% (from 16.9 APs to 2.6 APs, P < 0.001) in vagotomized NGNs. S imilar decreases in excitability were observed in vagotomized NGNs in intac t ganglia in vitro studied with "sharp" microelectrode techniques. Baseline electrophysiological properties and changes following vagotomy were simila r in right and left NGNs. A "sham" vagotomy procedure had no effect on NGN properties at 5 days, indicating that changes were due to severing the vagu s nerve itself, not surrounding tissue damage. NGNs isolated after being ma intained 17 h in vivo following vagotomy revealed no differences in excitab ility, suggesting that vagotomy-induced changes occur some time from 1-5 da ys after injury. Decreased excitability was still observed in NGNs isolated after 20-21 days in vivo following vagotomy. These data indicate that, in contrast to many primary sensory neurons that are thought to become hyperex citable following section of their axons, NGNs undergo a marked decrease in electrical excitability following vagotomy.