Increasing Intensity of Hypoxia Augments Fos Expression in Hypothalamic Paraventricular Nucleus (PVN)‐Projecting Neurons in the Nucleus of the Tractus Solitarius (nTS)

Abstract

Acute hypoxia (AH) activates peripheral chemoafferents. Sensory information is sent to the nTS, integrated and relayed to other brain regions to increase breathing, sympathetic nerve activity and blood pressure. The nTS sends direct projections to the PVN which may be excitatory or inhibitory, but the role of the projections in the chemoreflex is unknown. We used Fos‐immunoreactivity (IR) to determine activation of PVN‐projecting nTS neurons to AH. We hypothesized that increasing intensity of AH augments activation of nTS neurons, particularly PVN‐projecting cells. Fluorogold (FG) was microinjected bilaterally into the PVN to label nTS PVN‐projecting neurons (n=8 rats). After recovery, rats underwent normoxia (N, 21% O2) or AH (12, 10, or 8% O2; 3hr). Fos and GAD67 (marker for GABAergic cells) immunohistochemistry was performed. Positively labeled nTS neurons were counted. AH increased the number of Fos‐IR nTS cells (N, 15±0; 12%, 43±2; 10%, 157±49; 8%, 164±37). The percent of PVN‐projecting nTS cells co‐expressing Fos was greater at higher AH intensity (N, 3±0%; 12%, 11±2%; 10%, 32±12%; 8%, 30±4%). Fos‐IR was not altered by AH in GAD67‐IR cells. FG and GAD67 colabeling was low. Data suggest increasing AH intensity activates more nTS cells, especially non‐GAD67 PVN‐projecting neurons. The PVN may play an important role in cardiorespiratory responses as chemoreflex stimulation intensifies. HL55306, HL085108