# Recruitment principles and injury-induced plasticity in thoracic paravertebral sympathetic postganglionic neurons

> **NIH NIH R01** · EMORY UNIVERSITY · 2021 · $341,250

## Abstract

Project Summary
The present project explores a barely studied and poorly-understood area of vertebrate autonomic
neuroscience: the recruitment properties of thoracic paravertebral sympathetic postganglionic neurons
(tSPNs). The prominent role of thoracic paravertebral sympathetic chain ganglia is as the final neural control
element regulating vasomotor tone. Given their strategic nodal site in autonomic signaling to body, any
plasticity in tSPNs is likely to be of high significance. Unfortunately, tSPNs are largely inaccessible for in vivo
study, so operational principles are inferred from studies in cervical and lumbar chain ganglia. Only 3 in vitro
studies have revealed tSPN electrophysiological properties: none accurately measure cellular integrative
properties or underlying recruitment principles due to electrode impalement injury. We undertook the first
physiological studies on caudal thoracic chain ganglia in the adult mouse by developing an ex vivo preparation
with intact segmental preganglionic and rostrocaudal interganglionic connections. We obtained the first whole-
cell patch clamp recordings of tSPNs and observed fundamentally different integrative and firing properties are
than previously observed. This reliable data set is a critical prerequisite to realistic computational simulation.
We propose to interleave experimental testing with modeling to understand tSPN recruitment principles and
their integrative properties. [SA1] We will test the hypothesis that tSPNs have heterogeneous synaptic, cellular,
and network properties, and are active participants in input-output recruitment strategies.
Higher thoracic spinal cord injuries (SCI) disrupt the brainstem pathways that regulate tSPN excitability via
spinal preganglionic loops. Such disruption can lead to sudden life-threatening tSPN mediated hypertensive
crises (autonomic dysreflexia). Whether paravertebral sympathetic chain ganglia dysfunction contributes to
amplification in a vasomotor response is unknown. To fill this significant gap in knowledge, experimental
studies will disclose plasticity in the cellular and synaptic organizational rules serving tSPN recruitment. [SA2]
We will test the hypothesis that tSPNs increased their intrinsic excitability and convert from linear to non-linear
gain amplifiers after SCI. Computational simulation will construct a database amenable to realistic modeling of
recruitment principles of potential clinical relevance that could be transformative to the field. The relative
simplicity of the organization makes discovery of principles through modeling more assured than in more
complex systems. Realistic simulation of the neural bases of tSPN function and emergent dysfunction could
catalyze predictive drug discovery-based high throughput simulations that normalize function for rapid
preclinical testing.
Significance: we aim to uncover the operational principles governing the final neural command pathways
regulating vascular tone. As sympathetic hypera...

## Key facts

- **NIH application ID:** 10208977
- **Project number:** 5R01NS102871-05
- **Recipient organization:** EMORY UNIVERSITY
- **Principal Investigator:** SHAWN HOCHMAN
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2021
- **Award amount:** $341,250
- **Award type:** 5
- **Project period:** 2017-07-01 → 2023-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10208977

## Citation

> US National Institutes of Health, RePORTER application 10208977, Recruitment principles and injury-induced plasticity in thoracic paravertebral sympathetic postganglionic neurons (5R01NS102871-05). Retrieved via AI Analytics 2026-05-24 from https://api.ai-analytics.org/grant/nih/10208977. Licensed CC0.

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