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Hippocampal microcircuit dynamics probed using optical imaging approaches

机译:使用光学成像方法探查海马微电路动力学

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摘要

AbstractMammalian cortical structures are endowed with the capacity for plasticity, which emerges from a combination of the dynamics of circuit connectivity and function, and the intrinsic function of the neurons within the circuit. However, this capacity is accompanied by a significant risk: the capability to generate seizure discharges is also a property of all mammalian cortices. How do cortical circuits reconcile the requirement to maintain plasticity, but at the same time control seizure initiation? These issues come into particular focus in the hippocampus. The hippocampus is one of the main plasticity engines in the brain, and is also a structure frequently implicated in the generation of epileptic seizures, with temporal lobe epilepsy constituting the most prevalent form of epilepsy in the adult population. One aspect of hippocampal circuitry that is particularly prominent is its intimate interconnections with the entorhinal cortex. These interconnections create a number of excitatory synaptic loops within the limbic system, which, in addition to being important in cognitive function, can support reentrant activation and seizure generation. In the present review, using optical imaging approaches to elucidate circuit processing at high temporal and spatial resolution, we examine how two targets of entorhinal cortical input within the hippocampus, the dentate gyrus and area CA1, regulate these synaptic pathways in ways that can maintain functions important in generation of normal activity patterns, but that dampen the ability of these inputs to generate seizure discharges.
机译:摘要哺乳动物的皮质结构具有可塑性,这是由电路连通性和功能的动力学以及电路中神经元的固有功能共同产生的。但是,这种能力伴随着巨大的风险:产生癫痫发作放电的能力也是所有哺乳动物皮质的特性。皮质回路如何协调维持可塑性的要求,同时控制癫痫发作的发生?这些问题在海马中特别受到关注。海马是大脑中主要的可塑性引擎之一,并且也是经常与癫痫发作的发生有关的结构,颞叶癫痫是成年人中癫痫最普遍的形式。海马电路特别突出的一方面是其与内嗅皮层的紧密互连。这些相互联系在边缘系统内形成了许多兴奋性突触环,这些环除了在认知功能上很重要之外,还可以支持折返激活和癫痫发作。在本综述中,我们使用光学成像方法阐明了高时空分辨率下的电路处理,我们研究了海马内的内嗅皮质输入的两个目标(齿状回和CA1区)如何以维持功能的方式调节这些突触途径在正常活动模式的产生中起重要作用,但会削弱这些输入产生癫痫发作的能力。

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