ArticleAutonomic neuroscience : basic & clinical2026
Temperature and frequency dependence of conduction along sympathetic preganglionic axons.
Article in Autonomic neuroscience : basic & clinical, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed.
- Ion channel and receptor-mediated regulation of axonal conduction reliability in sympathetic preganglionic neurons.bioRxiv : the preprint server for biology · 2026Article
- Probabilistic spike propagation shapes sympathetic output in mouse preganglionic neurons.bioRxiv : the preprint server for biology · 2026Article
Corrections and comments
- Update of
Authors and funding
3 authors.
Funding
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.