Localization of Brain-Derived Neurotrophic Factor-Related Genes in the Rostral Ventrolateral Medulla of Male Sprague-Dawley Rats using RNAscope

Cardiovascular disease (CVD) is the leading cause of death in the US, and a large risk factor for CVD a sedentary lifestyle. CVD is often associated with increased activity of the sympathetic nervous system, which regulates blood pressure via vasoconstriction. Sedentary animals demonstrate increased activation of the sympathetic nervous following stimulation of a brainstem region known as the rostral ventrolateral medulla (RVLM). Similarly, sedentary versus active rats exhibit increased dendritic branching in the RVLM, suggesting a role for neurotrophic factors such as brain-derived neurotrophic factor (BDNF). While levels of mature BDNF protein are increased in the RVLM of sedentary rats, it is unclear whether BDNF neurons project to the RVLM or if BDNF is synthesized in the RVLM. The purpose of this study was to ascertain whether bdnf and related genes, trkb and p75 were localized in the RVLM. We hypothesize that bdnf will be expressed in the catecholamine (C1) neurons of the RVLM, which project to the spinal cord. We tested our hypothesis utilizing RNAscope™, a form of fluorescent in situ hybridization, and used confocal microscopy to locate bdnf, p75, and trkb in the RVLM of male Sprague-Dawley rats, using tyrosine hydroxylase ( th ) as a cell marker for C1 neurons. Preliminary results show that bdnf and trkb are expressed in C1 neurons in the RVLM, while p75 was highly expressed in non-C1 cells of the RVLM. These results support our initial hypothesis that bdnf is expressed in the C1 neurons of the RVLM, and suggest increased expression of BDNF in the RVLM may produce increased branching in the RVLM of sedentary rats. Further research into quantification of bdnf in C1 neurons under different conditions related to risk factors of CVD, e.g. rats with varying levels of physical activity, would provide greater insights into the mechanism of bdnf -mediated changes in sympathoexcitation. R01HL161233 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.