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Disinhibition in learning and memory circuits: New vistas for somatostatin interneurons and long-term synaptic plasticity

机译:在学习和记忆电路中解读:生长抑素型液面和长期突触可塑性的新Vistas

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摘要

Neural circuit functions involve finely controlled excitation/inhibition interactions that allow complex neuronal computations and support high order brain functions such as learning and memory. Disinhibition, defined as a transient brake on inhibition that favors excitation, recently appeared to be a conserved circuit mechanism implicated in various functions such as sensory processing, learning and memory. Although vasoactive intestinal polypeptide (VIP) interneurons are considered to be the main disinhibitory cells, recent studies highlighted a pivotal role of somatostatin (SOM) interneurons in inhibiting GABAergic interneurons and promoting principal cell activation. Interestingly, long-term potentiation of excitatory input synapses onto hippocampal SOM interneurons is proposed as a lasting mechanism for regulation of disinhibition of principal neurons. Such regulation of network metaplasticity may be important for hippocampal-dependent learning and memory.
机译:神经电路功能涉及精密控制的激励/抑制相互作用,其允许复杂的神经元计算并支持高阶大脑功能,例如学习和记忆。 禁止被定义为禁止激发的禁止瞬态制动,最近似乎是一种涉及各种功能的保守电路机制,例如感官处理,学习和存储器。 虽然血管活性肠道多肽(VIP)中间核被认为是主要的缺失细胞,但最近的研究强调了生长抑素(SOM)中间核抑制胃肠杆菌性核心和促进主要细胞活化的关键作用。 有趣的是,提出了在海马SOM中的兴奋性输入突触的长期潜力作为持久机制,用于监管主要神经元。 这种网络化塑料的调节对于海马依赖的学习和记忆可能是重要的。

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