Potentiation of the nicotinic acetylcholine receptor by aluminum in mammalian neurons

作者：Hu W P^*; Li X M; Chen J G; Li Z W

来源：Neuroscience, 2007, 149(1): 1-6.

DOI：10.1016/j.neuroscience.2007.07.018

• aluminum
• nicotinic acetylcholine receptor
• potentiation
• current
• neuron

Aluminum (Al3+), a known neurotoxic substance, has long been implicated in the pathogenesis of Alzheimer's disease and other neurodegenerative diseases. Al3+ targets many ligand-gated and voltage-gated ion channels and modulates their functions. In the present study, the actions of Al3+ on the nicotinic acetylcholine receptor (nAChR) were investigated by whole-cell patch clamp technique in acutely isolated rat trigeminal ganglion neurons. We observed that Al3+ potentiated nicotine-evoked inward currents in a concentration-dependent manner (10-1000 mu M). The effects of Al3+ on nicotine-evoked currents were voltage independent. Al3+ appeared to increase the affinity of nicotine to nAChR but not the efficacy. Al3+ reduced the agonist concentration producing a half-maximal response (EC50) for nicotine from 74.4 +/- 1.9 AM to 32.9 +/- 2.6 mu M, but did not alter the threshold nor maximal response. On the contrary, another trivalent cation, Ga3+, had little effect on nicotine-evoked currents. The present results indicated that A13+ enhanced the function of nAChR and this potentiation might underlie the neurological alteration induced by Al3+.

• 出版日期2007-10-12
• 单位华中科技大学; 湖北科技学院