Effects of Hypoxia on Fos Expression in RVLM‐Projecting Neurons in the Nucleus of the Solitary Tract (NTS)

Abstract

Peripheral chemosensory afferents responding to arterial oxygen levels terminate in the NTS, where afferent input is integrated, modified, and then sent to rostral ventrolateral medulla (RLVM) neurons. The cellular phenotype in the presumptive pathway remains largely unexplored. We hypothesized that hypoxia increases NTS neuronal activity primarily in RVLM‐projecting NTS cells. Rats (n=6) were microinjected with a fluorescent retrograde tracer into the RVLM, allowed to recover, and then exposed to normoxia (N) or hypoxia (H, 10% O2) for 3hr. Immunohistochemistry was performed using markers for neuronal activation (Fos) and catecholaminergic cells (tyrosine hydroxylase, TH). NTS neurons that were positive for Fos, TH, or tracer were counted unilaterally in 5 sections ±360 µm from calamus scriptorius. Hypoxia increased the number of Fos immunoreactive (IR) cells per section (H: 43±7 vs N: 5±1; p<0.05). In hypoxic rats 10±5% of Fos‐IR cells projected to the RVLM. In addition 12±1% of NTS cells expressing Fos were TH‐IR yet none of these projected to RVLM. Of RVLM‐projecting NTS cells, the percent that was Fos‐IR increased after hypoxia (H: 14±5 vs. N: 0±0%; p<0.05). A greater portion of TH‐IR cells also expressed Fos in hypoxic rats (H:23±1 vs N: 2±2%; p<0.05). Thus, hypoxia appears to increase neuronal activation in separate populations of catecholaminergic and RVLM projecting cells in the NTS. HL55306, HL085108