Exp Neurobiol 2005; 14(1): 1-4
Published online July 1, 2005
© The Korean Society for Brain and Neural Sciences
Ji-Hyun Noh and Jun-Mo Chung*
Department of Life Sciences and Center for Cell Signaling Research (CCSR), Ewha Womans University, Seoul 120-750, Korea
Correspondence to: *To whom correspondence should be addressed.
TEL: 82-2-3277-2395, FAX: 82-2-3277-2385
Aspirin, a well-known anti-inflammatory agent, is recently found to prevent Zn2+- mediated neuronal death by interfering with voltage-gated Ca2+ channels (VGCC). Here we employed a whole-cell voltage-clamp technique for cortical neurons acutely isolated from rat pups, in order to elucidate the mechanism by which aspirin modulates VGCC. Aspirin reduced high-threshold Ca2+ currents (HTCC) in a concentration-dependent manner. Aspirin did not affect voltage-dependency of either HTCC activation or inactivation. However, the gating kinetics of HTCC was altered by aspirin: time constants for activation were increased by aspirin whereas time constants for inactivation were decreased. Therefore, the reduction of HTCC by aspirin seems to result from slower activation and faster inactivation.
Keywords: acetyl salicylic acid, cortex, voltage-clamp, voltage-gated Ca2+ channels, whole cell recording