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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Integration of asynchronously released quanta prolongs the postsynaptic spike window.
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Integration of asynchronously released quanta prolongs the postsynaptic spike window.

机译：异步释放的量子的积分延长了突触后尖峰窗口。

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Classically, the release of glutamate in response to a presynaptic action potential causes a brief increase in postsynaptic excitability. Previous reports indicate that at some central synapses, a single action potential can elicit multiple, asynchronous release events. This raises the possibility that the temporal dynamics of neurotransmitter release may determine the duration of altered postsynaptic excitability. In response to physiological challenges, the magnocellular neurosecretory cells (MNCs) in the paraventricular nucleus of the hypothalamus (PVN) exhibit robust and prolonged increases in neuronal activity. Although the postsynaptic conductances that may facilitate this form of activity have been investigated thoroughly, the role of presynaptic release has been largely overlooked. Because the specific patterns of activity generated by MNCs require the activation of excitatory synaptic inputs, we sought to characterize the release dynamics at these synapses and determine whether they contributeto prolonged excitability in these cells. We obtained whole-cell recordings from MNCs in brain slices of postnatal day 21-44 rats. Stimulation of glutamatergic inputs elicited large and prolonged postsynaptic events that resulted from the summation of multiple, asynchronously released quanta. Asynchronous release was selectively inhibited by the slow calcium buffer EGTA-AM and potentiated by brief high-frequency stimulus trains. These trains caused a prolonged increase in postsynaptic spike activity that could also be eliminated by EGTA-AM. Our results demonstrate that glutamatergic terminals in PVN exhibit asynchronous release, which is important in generating large postsynaptic depolarizations and prolonged spiking in response to brief, high-frequency bursts of presynaptic activity.
机译：经典地，响应于突触前动作电位的谷氨酸的释放引起突触后兴奋性的短暂增加。先前的报告表明，在某些中央突触中，单个动作电位可能引发多个异步释放事件。这增加了神经递质释放的时间动态可能决定突触后兴奋性改变的持续时间的可能性。在应对生理挑战时，下丘脑室旁核（PVN）中的大细胞神经分泌细胞（MNC）表现出强劲而持久的神经元活性增加。尽管已经彻底研究了可能促进这种活动形式的突触后电导，但是突触前释放的作用已被大大忽略。由于由MNC产生的特定活动模式需要激活兴奋性突触输入，因此我们试图表征这些突触的释放动力学并确定它们是否有助于延长这些细胞的兴奋性。我们从产后21-44天的大鼠脑切片中的MNC获得了全细胞记录。谷氨酸能输入的刺激引起大量和长时间的突触后事件，这是由多个异步释放的量子的总和引起的。缓慢的钙缓冲液EGTA-AM选择性抑制了异步释放，并通过短暂的高频刺激增强了异步释放。这些火车导致突触后突波活动的延长，这也可以通过EGTA-AM消除。我们的研究结果表明，PVN中的谷氨酸能受体表现出异步释放，这在产生大的突触后去极化和响应突触前短暂的高频突触而产生的尖峰时很重要。

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