Khakh Baljit S
Department of Physiology, David Geffen School of Medicine, University of California Los Angeles, CA 90095-1751, USA.
Neuropharmacology. 2009 Jan;56(1):216-22. doi: 10.1016/j.neuropharm.2008.06.011. Epub 2008 Jun 14.
Previous work has shown that ATP-gated P2X2 receptors are expressed in excitatory nerve terminals onto stratum radiatum interneurons in the mouse hippocampal CA1 region. At these synapses receptor activation results in calcium-dependent facilitation of miniature and spontaneous EPSC frequency. In this study I determined if activation of presynaptic P2X receptors produces these effects by utilizing the vesicles underlying action potential dependent release. Brief trains of electrical stimuli caused short-term synaptic depression of excitatory synapses onto interneurons, in a manner consistent with depletion of the readily releasable pool of vesicles. P2X receptor activation increased the frequency of spontaneous EPSCs, but unexpectedly evoked little effect on synaptic depression. This suggests that P2X receptor activation does not markedly draw on the vesicles underlying action potential dependent glutamate release. However asynchronous EPSCs were increased following synaptic depression and a component of these appeared to be initiated by endogenously released ATP acting on presynaptic P2X receptors. Unexpectedly, the data suggest P2X receptor activation initiates a form of asynchronous glutamate release, rather than detectably affecting the vesicles underlying action potential evoked release.
先前的研究表明，ATP门控的P2X2受体在小鼠海马CA1区辐射层中间神经元的兴奋性神经末梢中表达。在这些突触处，受体激活导致微小和自发性兴奋性突触后电流（EPSC）频率的钙依赖性增强。在本研究中，我通过利用与动作电位依赖性释放相关的囊泡，确定突触前P2X受体的激活是否产生这些效应。短暂的电刺激串导致对中间神经元兴奋性突触的短期突触抑制，其方式与易释放囊泡池的耗尽一致。P2X受体激活增加了自发性EPSC的频率，但出乎意料的是对突触抑制几乎没有影响。这表明P2X受体激活并未显著利用与动作电位依赖性谷氨酸释放相关的囊泡。然而，在突触抑制后异步EPSC增加，其中一部分似乎是由内源性释放的ATP作用于突触前P2X受体引发的。出乎意料的是，数据表明P2X受体激活引发了一种异步谷氨酸释放形式，而不是可检测地影响与动作电位诱发释放相关的囊泡。
