Lung

, Volume 191, Issue 5, pp 445–447

Identification of the Nodose Ganglia and TRPV1 in Swine

  • Don HayesJr.
  • Kathleen K. Nicol
  • Joseph D. Tobias
  • Louis G. Chicoine
  • Victoria L. Duffy
  • Heidi M. Mansour
  • Thomas J. Preston
Article
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The vagal nerve is the tenth cranial nerve (CN) and is the only CN to extend through the neck into the thorax and abdomen. As a component of the autonomic nervous system, the vagal nerve innervates the visceral organs, including the lung. The majority of the bronchopulmonary sensory nerves are unmyelinated (C-fiber) afferents of the vagal nerve. The cell bodies of the visceral afferent fibers of the vagus nerve are located bilaterally in the inferior ganglion—also termed the nodose ganglia (NG). More recently, transient receptor potential vanilloid type 1 (TRPV1) channels have been identified and are expressed on the vagal C-fiber afferents, which play an important role in the cholinergic reflex pathway [1, 2, 3]. TRPV1 channels are nonselective cation channels and polymodal transducers that are known to be activated by increasing temperature, acidity (hydrogen ion), and endogenous inflammatory mediators [1, 2, 3].

Although differences exist between swine and human anatomy, the patterns of the vagal nerve are largely similar and closer in size than standard rodent models [4]. Data are limited on identifying autonomic neurons and associated cell bodies, including the NG in swine [5, 6]. The importance and study of pulmonary neurobiology in acute lung injury is gaining momentum and often requires the use of large animal models, including swine. With no previous reports of the identification and subsequent histopathologic confirmation of the NG and TRPV1 in swine, we provide our experiences in identifying the NG in common crossbred piglets used in an acute lung injury model investigating the benefits of extracorporeal membrane oxygenation. The vagal nerve was dissected based on anticipated location. Figure 1 outlines the two anatomical patterns of the vagal laryngeal branches as previously described by Ding et al. [4]. Figure 2 illustrates the NG structure of one animal on gross examination with this animal having anatomical pattern A from Fig. 1. Histopathologic assessment confirmed the NG on hematoxylin and eosin (H&E) staining (Fig. 3) and immunofluorescence staining for TRPV1 channels (Fig. 4).
Fig. 1

Two anatomical patterns of the vagal laryngeal branches in swine. aCLN cranial laryngeal nerve arising from the NG nodose ganglion with subsequent bifurcation into the ILN internal laryngeal nerve and ELN external laryngeal nerve. b Both the ILN and ELN branches directly from the cervical vagal nerve without a CLN trunk

Fig. 2

Gross examination of this animal demonstrating the vagal laryngeal nerve branches in an anatomic pattern that would be type A as illustrated in Fig. 1. The CLN cranial laryngeal nerve arises from the NG nodose ganglion that bifurcates into the ILN internal laryngeal nerve and ELN external laryngeal nerve. Incisions were performed in the dorsal neck, 4-6 cm inferior to the skull base

Fig. 3

A representative section of the vagal nerve nodose ganglion stained with H&E hematoxylin and eosin with associated nerve fibers in the adjacent soft tissue (magnification ×20)

Fig. 4

Immunofluorescence staining of TRPV1 channels in the nodose ganglion of swine (magnification ×20)

Nodose ganglia were successfully found with TRPV1 being identified in an efficient manner despite no previously reported methodology. Researchers in this area need to be aware of the anatomical variances of the vagal nerve and its laryngeal branches in swine. Future work is planned to address the neurobiology of the respiratory system during acute lung injury in this large animal model.

Notes

Acknowledgments

The authors thank Stacy Turpin for her assistance in the development of the illustration used in this manuscript.

Funding

Funding that supported this work was provided by The Research Institute of Nationwide Children’s Hospital.

Conflict of interest

The authors have no conflict of interest or disclosures related to any companies or organizations whose products or services that are discussed in this manuscript.

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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Don HayesJr.
    • 1
  • Kathleen K. Nicol
    • 2
  • Joseph D. Tobias
    • 3
  • Louis G. Chicoine
    • 1
  • Victoria L. Duffy
    • 4
  • Heidi M. Mansour
    • 5
  • Thomas J. Preston
    • 4
  1. 1.Department of PediatricsNationwide Children’s Hospital, The Ohio State University College of MedicineColumbusUSA
  2. 2.Department of PathologyNationwide Children’s Hospital, The Ohio State University College of MedicineColumbusUSA
  3. 3.Department of Anesthesiology and Pain MedicineNationwide Children’s Hospital, The Ohio State University College of MedicineColumbusUSA
  4. 4.Department of Cardiovascular PerfusionThe Heart Center, Nationwide Children’s HospitalColumbusUSA
  5. 5.Skaggs Center of Pharmaceutical Sciences, College of PharmacyThe University of Arizona-TucsonTucsonUSA

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