Mallika Halder, Yaqinq Li, Shawn Hochman
Sympathetic preganglionic neurons (SPNs) distribute signals across paravertebral ganglia, yet the reliability of spike propagation along their predominantly unmyelinated axons remains poorly defined. We examined temperature- and activity-dependent modulation of SPN axonal conduction in an ex vivo adult mouse thoracic sympathetic-chain preparation. Population compound action potentials (CAP) responses were evoked by supramaximal T10 ventral-root stimulation and recorded from the interganglionic nerve (IGN), which contains pathways that branch within the paravertebral chain, and the splanchnic nerve, presumed to project unbranching axons toward prevertebral ganglia. After scaling for temperature-dependent changes in conduction velocity and spike waveform, CAP magnitude at 36 °C was approximately 50% lower than at 22 °C, with preferential reduction of slower-conducting components. Reductions occurred in both pathways, indicating a shared vulnerability of small unmyelinated axons, whereas evidence for an additional branching-associated vulnerability was strongest during repetitive activation. Activity dependence was assessed using 20-s trains at 5 and 20 Hz. At 22 °C, slower-conducting components showed marked frequency-dependent depression that was greater in the IGN. Observed loss of individual units without change in spike amplitude support CAP depression as due to conduction block. At 36 °C, depression of slow components was not statistically detectable, faster-conducting components facilitated at 20 Hz, and several responses showed post-train potentiation. These differences may reflect temperature-dependent filtering of vulnerable slow-conducting axons rather than uniform changes in frequency-following properties. Thus, SPN axonal conduction is strongly modulated by temperature and activation history. Preferential vulnerability of slower-conducting, likely small-diameter axons identifies conduction reliability as a vulnerable site in sympathetic output.