Nanou Evanthia, Kyriakatos Alexandros, Bhattacharjee Arin, Kaczmarek Leonard K, Paratcha Gustavo, El Manira Abdeljabbar
Nobel Institute for Neurophysiology, Department of Neuroscience, Karolinska Institutet, SE-171 77 Stockholm, Sweden.
Proc Natl Acad Sci U S A. 2008 Dec 30;105(52):20941-6. doi: 10.1073/pnas.0806403106. Epub 2008 Dec 18.
Na(+)-activated K(+) (K(Na)) channels are expressed in neurons and are activated by Na(+) influx through voltage-dependent channels or ionotropic receptors, yet their function remains unclear. Here we show that K(Na) channels are associated with AMPA receptors and that their activation depresses synaptic responses. Synaptic activation of K(Na) channels by Na(+) transients via AMPA receptors shapes the decay of AMPA-mediated current as well as the amplitude of the synaptic potential. Thus, the coupling between K(Na) channels and AMPA receptors by synaptically induced Na(+) transients represents an inherent negative feedback mechanism that scales down the magnitude of excitatory synaptic responses.
钠激活钾(K(Na))通道在神经元中表达,并通过电压依赖性通道或离子型受体的钠内流而激活,但其功能仍不清楚。在这里,我们表明K(Na)通道与AMPA受体相关联,并且它们的激活会抑制突触反应。通过AMPA受体由钠瞬变对K(Na)通道进行突触激活,塑造了AMPA介导电流的衰减以及突触电位的幅度。因此,通过突触诱导的钠瞬变在K(Na)通道和AMPA受体之间的耦合代表了一种内在的负反馈机制,该机制可降低兴奋性突触反应的幅度。