Choi S, Lovinger D M
Department of Molecular Physiology and Biophysics, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-0615, USA.
J Neurosci. 1997 Nov 1;17(21):8613-20. doi: 10.1523/JNEUROSCI.17-21-08613.1997.
We have investigated the site of expression of striatal long-term synaptic depression (LTD) using analysis of Sr2+-induced asynchronous release of quanta from stimulated synapses. The cumulative amplitude distribution of Sr2+-induced asynchronous synaptic responses overlaps with that of miniature EPSCs (mEPSCs), suggesting that Sr2+-induced asynchronous responses are quantal. Quantal amplitude at stimulated synapses is not significantly altered after LTD induction, whereas quantal frequency decreases after LTD induction. The decrease in quantal frequency is prevented when LTD expression is blocked by dialyzing 10 mM EGTA into the postsynaptic neuron. Our findings are most consistent with the idea that expression of striatal LTD involves decreased neurotransmitter release with no change in quantal amplitude, despite the fact that induction of striatal LTD involves postsynaptic mechanisms.
我们利用对 Sr2+ 诱导的受刺激突触量子异步释放的分析,研究了纹状体长期突触抑制(LTD)的表达位点。Sr2+ 诱导的异步突触反应的累积幅度分布与微小兴奋性突触后电流(mEPSCs)的累积幅度分布重叠,表明 Sr2+ 诱导的异步反应是量子化的。在 LTD 诱导后,受刺激突触处的量子幅度没有显著改变,而量子频率在 LTD 诱导后降低。当通过向突触后神经元透析 10 mM 乙二醇双乙醚二胺四乙酸(EGTA)来阻断 LTD 表达时,量子频率的降低被阻止。我们的发现与以下观点最为一致,即纹状体 LTD 的表达涉及神经递质释放减少且量子幅度无变化,尽管纹状体 LTD 的诱导涉及突触后机制。