OBJECTIVETo investigate the neurotoxicity and its mechanism of quinolinic acid (QA) to spiral ganglion cells (SGC) and observe the protectable potential of MgCl(2) on SGC.

METHODSSGC were cultured in vitro for 72 h, and then were divided into 4 groups: control group, QA group (1 mmol/L QA), MK-801 group (1 mmol/L QA + 20 µmol/L MK-801)and MgCl(2) protected group (1 mmol/L QA + 1 mmol/L MgCl(2)). SGC apoptosis rate was analyzed by Annexin V staining and PI staining measurements after 24 h exposure to different medium. SGC cultured as methods above were divided into 4 groups as following: 100 µmol/L QA, 1 mmol/L QA, 20 µmol/L MK-801+1 mmol/L QA and 1 mmol/L MgCl(2) + 1 mmol/L QA. The intracellular calcium concentration was measured by laser scanning confocal microscope finally.

RESULTSApoptosis rate in QA group was higher than that in both of control group (59.1% ± 7.5% vs 9.2% ± 0.9%, x ± s, q = 11.9, P < 0.05) and MgCl(2) group (59.1% ± 7.5% vs 27.5% ± 8.3%, q = 7.5, P < 0.05). There was no significant difference between apoptosis rate of control and MK-801 group (12.8% ± 5.7% vs 9.2% ± 0.9%, q = 0.9, P > 0.05). It was shown that there was a significant increase of Ca(2+) in SGC in the presence of QA by laser scanning confocal microscope. MK-801 may completely block the increase of Ca(2+), and the increase of Ca(2+) can be reduce by the application of MgCl(2).

CONCLUSIONSQA might injure SGC by excessive activating NMDA receptors on the cell membrane. Mg(2+) may have the function to reduce the neurotoxicity of QA.