Are neuroepithelial bodies a part of pulmonary slowly adapting receptors?

TO THE EDITOR: I would like to congratulate Adriaensen and colleagues for their excellent works that contribute to the detailed morphology of neuroepithelial bodies (NEBs) (1–3). They form a structural basis for understanding NEB physiology. A very interesting thought proposed by the authors is that NEBs may be mechanosensors. To examine this issue, we injected flourescent dye into the nodose ganglia to show the sensory structures of NEBs (5) and slowly adapting receptors (SARs) (4) in the lung. We found their morphology is quite different. These neural tracing results were confirmed with histochemical staining (6), again showing that NEBs and SARs are two different entities. Na -K -ATPase-positive structures were not observed in NEBs, and NEBs seldom coexist with SARs. When seen together, only a small portion of the NEBs and SARs were in contact. Furthermore, tissue blocks containing SARs showed a receptor structure but not NEB structure after proper staining (6). Therefore, we concluded that generation of SAR activity is not dependent on information from the NEBs. Recently, Adriaensen et al. showed a beautiful picture (see Figure 3 in Ref. 1), with a smooth muscle receptor and a NEB in “close proximity.” In addition, they showed Na -K ATPase-immunoreactive (IR) structures within NEBs. This seemingly supports the NEB being a part of the SAR. Our conclusion differs. If the Na -K -ATPase-IR structure is a SAR in Fig. 3 (1), its activity could not be dependent on the nearby NEB, because the distance between them is 40–50 m. The gap is too large to have molecules released from the NEB effectively activate the SAR. We do not believe the Na -K ATPase-IR structures found in NEBs by Adriaensen et al. are SARs, because they are different entities. They have different locations, sizes, structures, and orientations and have different sensitivities to the Na -K -ATPase antibody. Their results (1–3) are consistent with ours (6), in that the NEB-related structures are less immune reactive to Na -K -ATPase antibody than the SARs. They showed that labeling of NEBrelated structures is not as strong as those in the smooth muscle, which are believed to be SARs. We did not detect Na -K -ATPase-IR structure in NEBs (6). The failure to reveal positive structures in NEBs was possibly due to our staining technique, which may not have been sensitive enough for whole mount staining. It can be difficult for the antibody to penetrate into deep structures. On the other hand, we can easily demonstrate structures in smooth muscle in the whole mount preparation, because SARs have stronger Na -K -ATPase expression. The SARs are very active and would be more abundant in Na -K -ATPase than NEBs, or any other airway sensory receptors, in order to achieve ionic redistribution. It is likely, as Adriaensen et al. imply, the myelinated axon directly connects with the NEB, probably originating from high-threshold A -receptor (HTAR) fibers (1). This is consistent with the fact that HTARs are much less active than SARs (5). Again, if the NEB does participate in the mechanotransduction of SARs, it must play a modulatory role.