Gordon Grant R J, Bains Jaideep S
Hotchkiss Brain Institute, Department of Physiology and Biophysics, University of Calgary, Calgary, Alberta, T2N 4N1, Canada.
J Neurosci. 2005 Dec 7;25(49):11385-95. doi: 10.1523/JNEUROSCI.2378-05.2005.
The origin of large-amplitude miniature EPSCs (mEPSCs) at central synapses remains to be firmly established. Here, we show that at excitatory synapses onto magnocellular neurosecretory cells in the hypothalamus, noradrenaline induces a rapid and robust increase in mEPSC amplitude that requires alpha1-adrenoceptor activation but is impervious to postsynaptic manipulations that block the putative insertion of AMPA receptors. In response to noradrenaline, mEPSCs exhibit a putative multimodal amplitude histogram distribution that is not attributable to random temporal summation, the unveiling of a quiescent synapse, or the release of large vesicles. Large-amplitude mEPSCs are sensitive to a high dose of ryanodine and are associated with an enhanced glutamate cleft concentration. Together, these data are consistent with the hypothesis that large-amplitude mEPSCs result from the synchronous release of multiple vesicles via rapid presynaptic calcium expulsion from intracellular stores.
中枢突触处大幅度微小兴奋性突触后电流(mEPSCs)的起源仍有待确切证实。在此,我们表明,在下丘脑大细胞神经分泌细胞的兴奋性突触处,去甲肾上腺素可诱导mEPSC幅度迅速且显著增加,这需要α1 - 肾上腺素能受体激活,但不受阻断AMPA受体假定插入的突触后操作的影响。对去甲肾上腺素的反应中,mEPSCs呈现出一种假定的多峰幅度直方图分布,这并非归因于随机的时间总和、静息突触的显露或大囊泡的释放。大幅度mEPSCs对高剂量的ryanodine敏感,且与谷氨酸裂隙浓度增加有关。总之,这些数据与以下假设一致:大幅度mEPSCs是通过细胞内钙库中突触前钙的快速排出导致多个囊泡同步释放的结果。