CALCINEURIN MEDIATES ENHANCED HIGH-VOLTAGE-ACTIVATED CALCIUM CURRENTS IN RAT PRIMARY CORTICAL NEURONS AFTER ACUTE HYPOXIA
Abstract number :
IW.73
Submission category :
1. Translational Research
Year :
2008
Submission ID :
9209
Source :
www.aesnet.org
Presentation date :
12/5/2008 12:00:00 AM
Published date :
Dec 4, 2008, 06:00 AM
Authors :
Kun Xiang, Elizabeth Tietz and L John Greenfield
Rationale: Acute regulation of ion channels by hypoxia has been associated with a variety of cellular responses linked to altered neuronal excitability. We evaluated the effects of transient hypoxia on voltage-gated calcium channels (VGCCs) in cultured rat primary cortical neurons (13-15 days in vitro). Methods: High-voltage activated (HVA) Ca2+ currents were acquired in whole-cell patch clamp recordings immediately after exposure to 1% O2 for 4 h or after recovery under normoxia (95% air / 5% CO2) for 48 h and compared to control. Results: A ~1.5-fold increase in maximal calcium current density (evoked at +5 mV) was detected immediately after hypoxia (normoxia: 14.1 ± 2.3 pA/pF, n=10 vs hypoxia: 20.4 ± 1.8 pA/pF, n=10, p<0.05) which reverted to baseline after 48 hr normoxic recovery (14.6 ± 3.3 pA/pF, n=7). The half-maximal potential of activation (normoxia: -0.8 ± 2.0 mV, n=10 vs hypoxia: -1.9 ± 3.7 mV, n=10, p>
Translational Research