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Identifying spinal sensory pathways activated by noxious esophageal acid
A M Harrington1, S M Brierley, N J Isaacs
1Nerve-Gut Research Laboratory, Discipline of Medicine, Faculty of Health Sciences, The University of Adelaide, Adelaide, South Australia, Australia; Department of Gastroenterology and Hepatology, Hanson Institute, Royal Adelaide Hospital, Adelaide, South Australia, Australia.
Neurogastroenterology and Motility
|July 16, 2013
Summary
The transient receptor potential vanilloid 1 (TRPV1) channel is crucial for sensing burning pain from the esophagus. This study shows TRPV1 significantly contributes to spinal signaling pathways activated by esophageal acid.
Area of Science:
- Neuroscience
- Pain Research
- Gastroenterology
Background:
- The transient receptor potential vanilloid 1 (TRPV1) channel mediates burning pain signals.
- Esophageal acid reflux is a common cause of burning pain.
- The role of TRPV1 in esophageal pain signaling is not well understood.
Purpose of the Study:
- Identify spinal afferent pathways for esophageal acid nociception.
- Determine the contribution of TRPV1 to these pathways.
Main Methods:
- Esophageal perfusion with acid/pepsin or saline/pepsin in wild-type and TRPV1 null mice.
- Immunolabeling for neuronal activation marker pERK in spinal cord and dorsal root ganglia (DRG).
- Characterization of responsive neurons using CGRP and IB4 markers.
Main Results:
- Esophageal acid perfusion significantly increased pERK-immunoreactive neurons in DRG and spinal cord dorsal horn.
- This increase was significantly attenuated in TRPV1 null mice.
- Identified specific neuronal populations (CGRP+, IB4+) involved in acid signaling.
Conclusions:
- Established spinal afferent pathways for esophageal acid nociception.
- Demonstrated a significant role for TRPV1 in mediating these pain signals.
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