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Chronic high inspired CO 2 decreases excitability of mouse hippocampal neurons
Author(s) -
Gu Xiang Q,
Kanaan Amjad,
Yao Hang,
Haddad Gabriel G
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.6.a925
Subject(s) - rheobase , hippocampal formation , chemistry , medicine , endocrinology , conductance , western blot , electrophysiology , patch clamp , biochemistry , mathematics , combinatorics , gene
To examine the effect of chronically elevated CO 2 on excitability and function of neurons, we exposed mice to 8% and 12% CO 2 for 4 weeks (starting at 2 days of age), and examined the properties of freshly dissociated hippocampal neurons obtained from slices. Chronic CO 2 ‐treated neurons (CC) had a similar input resistance (R m ) and resting membrane potential (V m ) as control (CON). While treatment with 8% CO 2 did not change the rheobase (64±11 pA, n=9 vs. 47±12 pA, n=8 for CC 8% vs. CON), 12% CO 2 treatment increased it significantly (73±8 pA, n=9, p=0.05). Furthermore, the 12% CO 2 but not the 8% CO 2 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% CO 2 . 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, II and III was not changed by 8% CO 2 treatment but their expression was significantly decreased by 20–30% (p=0.03) by the 12% treatment. We conclude from these data and others (Gu et al. 2004) that neuronal excitability and Na + channel expression depend on the duration and level of CO 2 exposure and maturational changes occur in early life regarding neuronal responsiveness to CO 2 . (This work was supported by NIH grants PO1 HD‐32573, RO1 NS‐35918 and RO1 HL‐66327).