摘要
突触前和突触后细胞内钙离子 ([Ca2 +]i)在短时程和长时程突触的可塑性中 ,发挥着重要的信息传递作用。兴奋后残留 [Ca2 +]i,可以激发短时程突触增强。突触前 [Ca2 +]i 可以影响被抑制的突触前膜囊泡的更新 ,并准确编码突触前和突触后信息 ,产生截然相反的长时程突触修饰 (LTP或LTD)。
Recent work shows that the intracellular free Ca 2+ concentrations ([Ca 2+ ] i) of the presynaptic and postsynaptic neurons play crucial signaling roles in short and long term synaptic plasticity. Residual [Ca 2+ ] i followed conditioning stimulation may cause short term synaptic enhancement. Presynaptic [Ca 2+ ] i could influence the replacing of presynaptic depressed vesicles, as well as encode the precise relative timing of presynaptic input and postsynaptic activity and generate long term synaptic modification of opposite polarity(LTP or LTD).
出处
《生理科学进展》
CAS
CSCD
北大核心
2001年第1期35-38,共4页
Progress in Physiological Sciences
基金
国家自然科学基金(39670259,3990080)
军队医药卫生科研基金(96M077,98M079)资助课题