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J Neurophysiol 97: 1833-1838, 2007. First published January 3, 2007; doi:10.1152/jn.01174.2006
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Chronic High-Inspired CO₂ Decreases Excitability of Mouse Hippocampal Neurons

¹Departments of Pediatrics, Section of Respiratory Medicine and ²Neuroscience, University of California; and ³The Rady's Children's Hospital, San Diego, California

Submitted 3 November 2006; accepted in final form 28 December 2006

To examine the effect of chronically elevated CO₂ on excitability and function of neurons, we exposed mice to 8 and 12% CO₂ for 4 wk (starting at 2 days of age), and examined the properties of freshly dissociated hippocampal neurons obtained from slices. Chronic CO₂-treated neurons (CC) had a similar input resistance (R_m) and resting membrane potential (V_m) as control (CON). Although treatment with 8% CO₂ did not change the rheobase (64 ± 11 pA, n = 9 vs. 47 ± 12 pA, n = 8 for CC 8% vs. CON; means ± SE), 12% CO₂ treatment increased it significantly (73 ± 8 pA, n = 9, P = 0.05). Furthermore, the 12% CO₂ but not the 8% CO₂ treatment decreased the Na⁺ channel current density (244 ± 36 pA/pF, n = 17, vs. 436 ± 56 pA/pF, n = 18, for CC vs. CON, P = 0.005). Recovery from inactivation was also lowered by 12% but not 8% CO₂. Other gating properties of Na⁺ current, such as voltage-conductance curve, steady-state inactivation, and time constant for deactivation, were not modified by either treatment. Western blot analysis showed that the expression of Na⁺ channel types I–III was not changed by 8% CO₂ treatment, but their expression was significantly decreased by 20–30% (P = 0.03) by the 12% treatment. We conclude from these data and others that neuronal excitability and Na⁺ channel expression depend on the duration and level of CO₂ exposure and maturational changes occur in early life regarding neuronal responsiveness to CO₂.

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