Submitted on June 16, 2005
Revised on September 19, 2005
Accepted on September 30, 2005
Inhibitory effect of ganglioside GD1b on K+ current in hippocampal neurons and its involvement in cell apoptosis suppression
Xuesong Chen, Shaopeng Chi, Mingna Liu, Wei Yang, Taotao Wei, Zhi Qi, and Fuyu Yang
State Key Laboratory of Brain and Cognitive Science, Institute of Biophysics, Beijing 100101
Corresponding Author: qizhi{at}sun5.ibp.ac.cn
Gangliosides are endogenous membrane components enriched in neuronal cells. They have been shown to play regulatory roles in many cellular processes. Here, we show for the first time that ganglioside GD1b plays an anti-apoptotic role in cultured hippocampal neurons. GD1b inhibited the outward delayed rectifier IK current but not the transient outward IA current in a dose-dependent manner with IC50 value of 15.2
M. Such effect appears to be somehow specific, since GD1b, but not GM1, GM2, GM3, GD1a, GD3 or GT1b, was effective on inhibiting IK current. Intracellular application of STS (0.1
M) resulted in rapid activation of IK, which was partially reversed upon addition of K+ channel blocker tetraethylammonium (TEA, 5 mM) and GD1b (10
M). Furthermore, GD1b (10
M) attenuated staurosporine-induced neuronal apoptosis by nearly the same as that of 5 mM TEA. In addition, GD1b suppressed the apoptosis-associated capase 3 activation that was activated by STS. Collectively, these findings implicate that GD1b plays an anti-apoptotic role in cultured hippocampal neurons through its inhibitory effect on the outward IK current and the caspase activity.