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Bidirectional plasticity of excitatory postsynaptic potential (EPSP)-spike coupling in CA1 hippocampal pyramidal neurons

机译:CA1海马锥体神经元的兴奋性突触后电位(EPSP)-峰值耦合的双向可塑性

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Integration of synaptic excitation to generate an action potential (excitatory postsynaptic potential-spike coupling or E-S coupling) determines the neuronal output. Bidirectional synaptic plasticity is well established in the hippocampus, but whether active synaptic integration can display potentiation and depression remains unclear. We show here that synaptic depression is associated with an N-methyl-D-aspartate receptor-dependent and long-lasting depression of E-S coupling. E-S depression is input-specific and is expressed in the presence of γ-aminobutyric acid type A and B receptor antagonists. In single neurons, E-S depression is observed without modification of postsynaptic passive properties. We conclude that a decrease in intrinsic excitability underlies E-S depression and is synergic with gluta-matergic long-term depression.
机译:突触兴奋的整合以产生动作电位(兴奋性突触后电位峰值耦合或E-S耦合)决定了神经元输出。在海马中已经建立了双向突触可塑性,但是尚不清楚主动突触整合是否可以显示增强和抑制作用。我们在这里显示,突触抑制与N-甲基-D-天冬氨酸受体依赖性和E-S耦合的长期抑制有关。 E-S抑郁症是特定于输入的,在存在A和B型γ-氨基丁酸受体拮抗剂的情况下表达。在单个神经元中,观察到E-S抑郁而未改变突触后被动特性。我们得出的结论是,内在兴奋性的降低是E-S抑郁症的基础,并且与谷氨酸持续性抑郁症具有协同作用。

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