Carotid body of transgenic mice with nicotinic ACh receptor a3 subunit deletion

Abstract

The carotid body (CB) detects the arterial partial pressure of O2 and CO2. Previous studies suggested that nicotinic ACh receptors (nAChRs) play a role in these processes. We investigated if deletion of the nAChR α3 subunit influences gene expression, morphology and function of the CB in 2 week old mice. Real‐time PCR analysis was performed on CB from wild type (WT), heterozygous (HET), and knockout (KO) mice. Cholinergic traits (enzymes for ACh metabolism and receptors) were well preserved in all mice, except for the α3 subunit in KO mice. Dopaminergic traits and BK channels were down regulated in KO mice. Morphometry studies were performed in plastic embedded and serial‐sectioned CBs. The volumes and cell morphology between WT and HET CBs were similar. CB function was assessed by the ventilatory response to short exposures of 100% O2 and 15% O2 using whole body plethysmography. Both WT and HET have similar ventilatory responses to hyperoxia and hypoxia, hypoventilating in response to hyperoxia and hyperventilating in response to hypoxia. The results suggest that the α3 subunit is linked to the expression of BK channels and dopaminergic traits in the CB. Similarities between the phenotypes of WT and HET mice may be due to compensation occurring in the HET.Supported by HL72293. Transgenic mice were originally provided by Dr. De Biasi, Baylor College of Medicine.