海马体CA1区锥体神经元中兴奋性突触后电位（EPSP）-峰电位耦合的双向可塑性。
Bidirectional plasticity of excitatory postsynaptic potential (EPSP)-spike coupling in CA1 hippocampal pyramidal neurons.
作者信息
Daoudal Gael, Hanada Yasuhiro, Debanne Dominique
机构信息
Neurobiologie des Canaux Ioniques, Institut National de la Santé et de la Recherche Médicale U464, Institut Fédératif de Recherche Jean Roche, Université de la Méditerranée, Bd P. Dramard, 13916 Marseille cedex 20, France.
出版信息
Proc Natl Acad Sci U S A. 2002 Oct 29;99(22):14512-7. doi: 10.1073/pnas.222546399. Epub 2002 Oct 21.
Abstract
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 gamma-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 glutamatergic long-term depression.
摘要
突触兴奋的整合以产生动作电位（兴奋性突触后电位-峰电位耦合或E-S耦合）决定了神经元的输出。双向突触可塑性在海马体中已得到充分证实，但活跃的突触整合是否能表现出增强和抑制尚不清楚。我们在此表明，突触抑制与N-甲基-D-天冬氨酸受体依赖性和E-S耦合的持久抑制有关。E-S抑制是输入特异性的，并且在存在A型和B型γ-氨基丁酸受体拮抗剂的情况下表现出来。在单个神经元中，观察到E-S抑制而突触后被动特性未发生改变。我们得出结论，内在兴奋性的降低是E-S抑制的基础，并且与谷氨酸能长时程抑制协同作用。
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