Further evidence of redox modulation of neurons in a CO2‐chemosensitive area: normobaric hyperoxia (95%O2) stimulates CO2‐chemosensitive and –insensitive neurons in the solitary complex (SC)

Abstract

We previously reported that CO2‐excited neurons in SC, in medullary slices maintained in 95%O2, are stimulated by chemical oxidants and hyperbaric O2 (JAP 95:910‐921, 2003; AJP 286:C940–951, 2004). Here we test the hypothesis that SC neurons, maintained in 40%O2 rather than 95%O2 (to reduce oxidative stress), are viable and stimulated by normobaric hyperoxia (95%O2). Slices (P1–21) were harvested in chilled ACSF gassed with 95%O2 and immediately transferred to ACSF (22–24°C) equilibrated with 40%O2‐5%CO2 in N2. Whole cell recordings (35–37°C) were established in 40%O2 (n=44) and tested using hyperoxia (40→95%O2) and hypercapnia (5→10 or 15%CO2). Hyperoxia stimulated 8/44 neurons and hypercapnia stimulated 5/44 neurons; of these 4/8 were stimulated by both O2 and CO2. Hyperoxia usually increased firing rate and decreased input resistance whereas hypercapnia increased firing rate and input resistance. Most neurons tested were insensitive to hyperoxia and hypercapnia (31/44). Compared to previous slice studies that used 95%O2 control, there is a smaller proportion of CO2‐excited SC neurons in slices maintained in 40%O2. These data indicate that medullary slices are viable in 40%O2 and that hyperoxic stress stimulates SC neurons, including CO2‐excited neurons. These data also suggest that oxidative stimuli increases the incidence of CO2‐chemosensitivity in SC neurons (ONR N000140110179, NIH R01HL56683)