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首页> 外文期刊>Journal of Neurophysiology >Activity-dependent long-term potentiation of electrical synapses in the mammalian thalamus.
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Activity-dependent long-term potentiation of electrical synapses in the mammalian thalamus.

机译：哺乳动物丘脑中电突触的活动依赖性长期增强。

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Activity-dependent changes of synapse strength have been extensively characterized at chemical synapses, but the relationship between physiological forms of activity and strength at electrical synapses remains poorly characterized and understood. For mammalian electrical synapses comprising hexamers of connexin36, physiological forms of neuronal activity in coupled pairs have thus far only been linked to long-term depression; activity that results in strengthening of electrical synapses has not yet been identified. Here, we performed dual whole-cell current-clamp recordings in acute slices of P11-P15 Sprague-Dawley rats of electrically coupled neurons of the thalamic reticular nucleus (TRN), a central brain area that regulates cortical input from and attention to the sensory surround. Using TTA-A2 to limit bursting, we show that tonic spiking in one neuron of a pair results in long-term potentiation of electrical synapses. We use experiments and computational modeling to show that the magnitude of plasticity expressed alters the functionality of the synapse. Potentiation is expressed asymmetrically, indicating that regulation of connectivity depends on the direction of use. Furthermore, calcium pharmacology and imaging indicate that potentiation depends on calcium flux. We thus propose a calcium-based activity rule for bidirectional plasticity of electrical synapse strength. Because electrical synapses dominate intra-TRN connectivity, these synapses and their activity-dependent modifications are key dynamic regulators of thalamic attention circuitry. More broadly, we speculate that bidirectional modifications of electrical synapses may be a widespread and powerful principle for ongoing, dynamic reorganization of neuronal circuitry across the brain. NEW & NOTEWORTHY This work reveals a physiologically relevant form of activity pairing in coupled neurons that results in long-term potentiation of mammalian electrical synapses. These findings, in combination with previous work, allow the authors to propose a bidirectional calcium-based rule for plasticity of electrical synapses, similar to those demonstrated for chemical synapses. These new insights inform the field on how electrical synapse plasticity may modify the neural circuits that incorporate them.
机译：在化学突触中，突触强度的活动依赖性变化已被广泛描述，但在电突触中，活动的生理形式与强度之间的关系仍然缺乏描述和理解。对于包含连接蛋白36六聚体的哺乳动物电突触，迄今为止，成对神经元活动的生理形式仅与长期抑郁有关；导致电突触增强的活动尚未确定。在这里，我们在P11-P15 Sprague-Dawley大鼠的急性脑片中，对丘脑网状核（TRN）的电耦合神经元进行了双全细胞电流钳制记录。TRN是一个中央大脑区域，调节来自感觉周围的皮质输入和注意。使用TTA-A2来限制爆发，我们证明了一对神经元中的一个神经元中的强直脉冲会导致电突触的长时程增强。我们通过实验和计算模型证明，表达的可塑性的大小改变了突触的功能。增强作用的表达是不对称的，这表明连接性的调节取决于使用的方向。此外，钙药理学和影像学表明，增强作用取决于钙通量。因此，我们提出了一个基于钙的电突触强度双向可塑性活动规则。由于电突触主导着TRN内的连接，这些突触及其活动依赖性修饰是丘脑注意回路的关键动态调节器。更广泛地说，我们推测，电突触的双向修饰可能是一个广泛而有力的原理，可以持续、动态地重组大脑中的神经回路。新的和值得注意的这项工作揭示了耦合神经元中一种生理相关的活动配对形式，导致哺乳动物电突触的长时程增强。这些发现，结合之前的工作，允许作者提出一个双向钙基规则，用于电突触的可塑性，类似于化学突触的可塑性。这些新的见解为该领域提供了关于电突触可塑性如何改变包含它们的神经回路的信息。

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