Objective：The effects of nifedipine on the release of amino acids and free calcium concentrations ([Ca2+ ]i) from ischemic synaptosomes were investigated in order to explore the relationship between its protective action against brain injury induced by ischemia and its influence on [Ca2+ ]i as well as release of excitatory amino acids (EAA) and inhibitory amino acids (IAA). Methods：Ischemic synaptosome model was established by substration of glucose and oxygen from synaptosome suspension. The release of EAA

IAA and [Ca2+ ]i from or in ischemic synaptosomes were determined under the conditions of either resting or stimulation of 50 mmol/L K+. Results: Ischemic condition induced [Ca2+ ]i increase in both resting and 50mmol/L K+- stimulated synaptosomes. Obviously it caused more release of aspartate

glutamate

glycine

taurine

GABA from 50 mmol/L K+- stimulated synaptosomes than resting synaptosomes. 10-4 mol/L nifedipine not only reduced the [Ca2+ ]i increase

but also decreased the release of aspartate

glutamate

and glycine

taurine

GABA in ischemic synaptosomes. Conclusion：The neuronal protection of nifedipine against brain damage induced by ischemia is related to inhibiting calcium influx. However

whether the protective effect of nifedipine is related to simultaneously blocking release of EAA and IAA needs further illustration.