Blackman Arne V, Abrahamsson Therese, Costa Rui Ponte, Lalanne Txomin, Sjöström P Jesper
Department of Neuroscience, Physiology and Pharmacology, University College London London, UK.
Department of Neurology and Neurosurgery, Centre for Research in Neuroscience, The Research Institute of the McGill University Health Centre, Montreal General Hospital Montreal, QC, Canada.
Front Synaptic Neurosci. 2013 Dec 6;5:11. doi: 10.3389/fnsyn.2013.00011.
Short-term plasticity (STP) denotes changes in synaptic strength that last up to tens of seconds. It is generally thought that STP impacts information transfer across synaptic connections and may thereby provide neurons with, for example, the ability to detect input coherence, to maintain stability and to promote synchronization. STP is due to a combination of mechanisms, including vesicle depletion and calcium accumulation in synaptic terminals. Different forms of STP exist, depending on many factors, including synapse type. Recent evidence shows that synapse dependence holds true even for connections that originate from a single presynaptic cell, which implies that postsynaptic target cell type can determine synaptic short-term dynamics. This arrangement is surprising, since STP itself is chiefly due to presynaptic mechanisms. Target-specific synaptic dynamics in addition imply that STP is not a bug resulting from synapses fatiguing when driven too hard, but rather a feature that is selectively implemented in the brain for specific functional purposes. As an example, target-specific STP results in sequential somatic and dendritic inhibition in neocortical and hippocampal excitatory cells during high-frequency firing. Recent studies also show that the Elfn1 gene specifically controls STP at some synapse types. In addition, presynaptic NMDA receptors have been implicated in synapse-specific control of synaptic dynamics during high-frequency activity. We argue that synapse-specific STP deserves considerable further study, both experimentally and theoretically, since its function is not well known. We propose that synapse-specific STP has to be understood in the context of the local circuit, which requires combining different scientific disciplines ranging from molecular biology through electrophysiology to computer modeling.
短期可塑性（STP）指的是持续长达数十秒的突触强度变化。一般认为，STP会影响突触连接间的信息传递，从而可能赋予神经元一些能力，比如检测输入连贯性、维持稳定性以及促进同步性。STP是多种机制共同作用的结果，包括突触小泡耗竭和突触终末的钙积累。根据包括突触类型在内的多种因素，存在不同形式的STP。最近的证据表明，即使对于源自单个突触前细胞的连接，突触依赖性依然成立，这意味着突触后靶细胞类型可以决定突触的短期动态。这种情况令人惊讶，因为STP本身主要是由突触前机制引起的。靶标特异性突触动态还意味着，STP并非是突触因过度激活而疲劳导致的缺陷，而是大脑为了特定功能目的而选择性实现的一种特征。例如，靶标特异性STP会在高频放电期间导致新皮层和海马兴奋性细胞出现顺序性的体细胞和树突抑制。最近的研究还表明，Elfn1基因在某些突触类型中特异性地控制STP。此外，突触前NMDA受体在高频活动期间对突触动态的突触特异性控制中也发挥了作用。我们认为，突触特异性STP无论在实验上还是理论上都值得进一步深入研究，因为其功能尚不清楚。我们提出，必须在局部回路的背景下理解突触特异性STP，这需要结合从分子生物学、电生理学到计算机建模等不同的科学学科。
