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Stressor-Selective Sympathetic Preganglionic Modules for Organ-Biased Control

The sympathetic nervous system coordinates organ function during stress, yet the spinal organization that converts autonomic commands into selective peripheral outputs remains poorly understood. Here, we combined spatial transcriptomics, immediate early gene mapping, anatomical tracing, and functional perturbation to define the cellular logic of spinal sympathetic preganglionic neurons (SPNs) in…

The sympathetic nervous system plays a crucial role in coordinating organ function during stressful situations. However, the specific spinal organization that translates autonomic commands into targeted peripheral responses is not well understood. To address this gap, researchers have combined various techniques to decipher the cellular logic of spinal sympathetic preganglionic neurons (SPNs) in mice.

By analyzing spatial transcriptomics, immediate early gene mapping, anatomical tracing, and functional perturbation, they have identified distinct cellular subtypes of SPNs that are organized by spinal segment and sex. These subtypes respond differently to physiological stressors, forming stressor-selective sympathetic output modules.

In particular, neurotensin-expressing (Nts+) SPNs in the lower thoracic spinal cord were found to have a unique role in managing cold stress. These cells create a specialized output channel to the lower sympathetic trunk and aorticorenal ganglia, which helps regulate the mobilization of white adipose tissue lipids in a female-biased manner.

Importantly, Nts+ SPNs are essential for cold tolerance when food is not readily available. This research establishes a cell-type-resolved spinal architecture that connects physiological demands to organ-specific sympathetic output, highlighting the preganglionic layer as a critical organizer of brain-body control.

Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.

Read the original at biorxiv.org →

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