Acute hypoxia (AH) augments Fos expression in hypothalamic paraventricular nucleus (PVN)‐projecting neurons in the caudal ventrolateral medulla (CVLM)

Hypoxia activates catecholamine neurons in the CVLM. The PVN modulates arterial chemoreflex responses and receives catecholaminergic projections from the CVLM, but it is not known whether the CVLM‐PVN projection is activated by chemoreflex stimulation. We hypothesized that AH preferentially activates PVN‐projecting catecholaminergic neurons in the CVLM. Fluorogold (FG, 2%, 60–90nL) was microinjected into the PVN to retrogradely label CVLM neurons. After recovery, conscious rats underwent 3 hrs of normoxia (N:21% O2, n=3) or AH (10% O2, n=4). We used Fos‐immunoreactivity (IR) as an index of CVLM neuronal activation and tyrosine hydroxylase (TH‐IR) to identify catecholaminergic neurons. Positively labeled neurons were counted in 6 sections containing CVLM. Approximately 40% of PVN projecting CVLM neurons were catecholaminergic. AH increased the number of Fos‐IR CVLM cells (N: 21 ± 10; AH: 123 ± 7; p<0.001). After AH, 36±7% of PVN projecting cells were activated and the majority of these (81%±6) were also catecholaminergic. 71±7% of catecholaminergic cells were activated after AH and 43%±3 of these also projected to the PVN. Of all PVN projecting catecholaminergic cells, 76±4% was activated by AH. Data suggest AH preferentially activates catecholaminergic, PVN‐projecting CVLM neurons. These neurons may be important in the cardiorespiratory responses elicited by the chemoreflex. HL55306, 85108, 98602.