Immunohistochemical Changes in 5 Respiratory Nuclei after Bilateral Carotid Body Denervation (CBD) in Sprague Dawley Rats

Abstract

Bilateral CBD in rat has no effect on CO2 sensitivity but elicits hypoventilation 1–2 d post‐CBD followed by a return to baseline values 7–8 d post‐CBD. To investigate the neural mechanisms driving the recovery of breathing after CBD, we compared NK1 receptor staining intensity on neuronal membranes from 5 different respiratory nuclei (solitary tract, NTS; dorsal motor, DMV; hypoglossal, nXII; nucleus ambiguous, NA; pre‐botzinger complex, PBC). Brain tissue was obtained from sham (n=1) and CBD animals sacrificed 4–5 (n=1), and >;21 d (n=2) post‐CBD. Optical density (OD) measurements of NK1 in NTS, DMV, and nXII in the sham rat (0.91, 0.96, 0.80 OD, respectively) were similar to rats sacrificed after 21 d post CBD (0.84, 0.96, 0.74 OD, respectively). The rat sacrificed 4–5 d post‐CBD had less intense NK1 staining in the NTS (0.68 OD), DMV (0.77 OD), and nXII (0.65 OD) relative to the other group of rats. The sham rat had lower OD values in the NA (0.54 OD) and PBC (0.70 OD) than rats sacrificed after 21 d post‐CBD (0.93 and 0.93 OD, respectively). These preliminary data suggest that CBD causes a down‐regulation, and recovery from CBD due to up‐regulation of the NK1 receptor. Remaining tissue sections from the same animals will be used to compare AMPA type 2, NMDA type 1, the serotonin transporter, and 5HT2A receptor staining intensities in the same respiratory nuclei. Supported by NIH HL097033