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Neuroepithelial bodies: a morphologic substrate for the link between neuronal nitric oxide and sensitivity to airway hypoxia?
J Comp Neurol. 2002 Aug 05; 449(4):343-54.JC

Abstract

Currently, the significance of nitric oxide (NO) in the respiratory tract is a matter of great interest because NO is believed to play a major role in the physiological regulation of airway function but also in lung pathology. What is especially intriguing with respect to the present investigation, are reports that the pulmonary expression of neuronal NO synthase (nNOS) is altered as a result of airway hypoxia. We examined the possible relationship between intrapulmonary nitrergic structures and pulmonary neuroepithelial bodies (NEBs), chemoreceptor-like epithelial cell groups that are known to have all necessary components for oxygen perception. Tyramide-enhanced immunostaining for nNOS was combined with known markers for NEBs in an ontogenetic study of rat lungs. From postnatal day 2 onward, nNOS-immunoreactive (-IR) neuronal cell bodies, present mainly in the lamina propria at all levels of intrapulmonary airways, were seen to give rise to remarkable intraepithelial terminal arborizations that invariably colocalized with NEBs. nNOS immunoreactivity was absent from the vagal calbindin D28k(CB) -IR and the spinal calcitonin gene-related peptide(CGRP) -IR extrinsic sensory nerve fiber populations that our group reported earlier to selectively contact NEBs. Quantitative analysis showed that all NEBs receiving nNOS-IR terminals were also contacted by CGRP-IR nerve fibers, whereas approximately 55% were additionally contacted by CB-IR nerves. The reported nitrergic neurons did not express the cholinergic marker vesicular acetylcholine transporter and were always surrounded by a basket of CGRP-IR nerve terminals. In conclusion, part of the pulmonary NEBs selectively receive extensive nitrergic nerve terminals that originate from intrinsic neurons. Together with literature data on lung physiology and pharmacology, some interesting suggestions for the functional significance of the association between pulmonary CGRP-IR NEBs, nNOS-IR neurons, and CGRP-IR afferents described in the present study, are discussed.

Authors+Show Affiliations

Laboratory of Cell Biology and Histology, University of Antwerp (RUCA), Groenenborgerlaan 171, B-2020 Antwerp, Belgium.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12115670

Citation

Brouns, Inge, et al. "Neuroepithelial Bodies: a Morphologic Substrate for the Link Between Neuronal Nitric Oxide and Sensitivity to Airway Hypoxia?" The Journal of Comparative Neurology, vol. 449, no. 4, 2002, pp. 343-54.
Brouns I, Van Genechten J, Scheuermann DW, et al. Neuroepithelial bodies: a morphologic substrate for the link between neuronal nitric oxide and sensitivity to airway hypoxia? J Comp Neurol. 2002;449(4):343-54.
Brouns, I., Van Genechten, J., Scheuermann, D. W., Timmermans, J. P., & Adriaensen, D. (2002). Neuroepithelial bodies: a morphologic substrate for the link between neuronal nitric oxide and sensitivity to airway hypoxia? The Journal of Comparative Neurology, 449(4), 343-54.
Brouns I, et al. Neuroepithelial Bodies: a Morphologic Substrate for the Link Between Neuronal Nitric Oxide and Sensitivity to Airway Hypoxia. J Comp Neurol. 2002 Aug 5;449(4):343-54. PubMed PMID: 12115670.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neuroepithelial bodies: a morphologic substrate for the link between neuronal nitric oxide and sensitivity to airway hypoxia? AU - Brouns,Inge, AU - Van Genechten,Jeroen, AU - Scheuermann,Dietrich W, AU - Timmermans,Jean-Pierre, AU - Adriaensen,Dirk, PY - 2002/7/13/pubmed PY - 2002/8/29/medline PY - 2002/7/13/entrez SP - 343 EP - 54 JF - The Journal of comparative neurology JO - J. Comp. Neurol. VL - 449 IS - 4 N2 - Currently, the significance of nitric oxide (NO) in the respiratory tract is a matter of great interest because NO is believed to play a major role in the physiological regulation of airway function but also in lung pathology. What is especially intriguing with respect to the present investigation, are reports that the pulmonary expression of neuronal NO synthase (nNOS) is altered as a result of airway hypoxia. We examined the possible relationship between intrapulmonary nitrergic structures and pulmonary neuroepithelial bodies (NEBs), chemoreceptor-like epithelial cell groups that are known to have all necessary components for oxygen perception. Tyramide-enhanced immunostaining for nNOS was combined with known markers for NEBs in an ontogenetic study of rat lungs. From postnatal day 2 onward, nNOS-immunoreactive (-IR) neuronal cell bodies, present mainly in the lamina propria at all levels of intrapulmonary airways, were seen to give rise to remarkable intraepithelial terminal arborizations that invariably colocalized with NEBs. nNOS immunoreactivity was absent from the vagal calbindin D28k(CB) -IR and the spinal calcitonin gene-related peptide(CGRP) -IR extrinsic sensory nerve fiber populations that our group reported earlier to selectively contact NEBs. Quantitative analysis showed that all NEBs receiving nNOS-IR terminals were also contacted by CGRP-IR nerve fibers, whereas approximately 55% were additionally contacted by CB-IR nerves. The reported nitrergic neurons did not express the cholinergic marker vesicular acetylcholine transporter and were always surrounded by a basket of CGRP-IR nerve terminals. In conclusion, part of the pulmonary NEBs selectively receive extensive nitrergic nerve terminals that originate from intrinsic neurons. Together with literature data on lung physiology and pharmacology, some interesting suggestions for the functional significance of the association between pulmonary CGRP-IR NEBs, nNOS-IR neurons, and CGRP-IR afferents described in the present study, are discussed. SN - 0021-9967 UR - https://www.unboundmedicine.com/medline/citation/12115670/Neuroepithelial_bodies:_a_morphologic_substrate_for_the_link_between_neuronal_nitric_oxide_and_sensitivity_to_airway_hypoxia L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0021-9967&date=2002&volume=449&issue=4&spage=343 DB - PRIME DP - Unbound Medicine ER -