O'Brien R J, Kamboj S, Ehlers M D, Rosen K R, Fischbach G D, Huganir R L
Howard Hughes Medical Institute, Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Neuron. 1998 Nov;21(5):1067-78. doi: 10.1016/s0896-6273(00)80624-8.
Both theoretical and experimental work have suggested that central neurons compensate for changes in excitatory synaptic input in order to maintain a relatively constant output. We report here that inhibition of excitatory synaptic transmission in cultured spinal neurons leads to an increase in mEPSC amplitudes, accompanied by an equivalent increase in the accumulation of AMPA receptors at synapses. Conversely, increasing excitatory synaptic activity leads to a decrease in synaptic AMPA receptors and a decline in mEPSC amplitude. The time course of this synaptic remodeling is slow, similar to the metabolic half-life of neuronal AMPA receptors. Moreover, inhibiting excitatory synaptic transmission significantly prolongs the half-life of the AMPA receptor subunit GluR1, suggesting that synaptic activity modulates the size of the mEPSC by regulating the turnover of postsynaptic AMPA receptors.
理论和实验研究均表明，中枢神经元会补偿兴奋性突触输入的变化，以维持相对恒定的输出。我们在此报告，在培养的脊髓神经元中抑制兴奋性突触传递会导致微小兴奋性突触后电流（mEPSC）幅度增加，同时突触处AMPA受体的积累也会等量增加。相反，增加兴奋性突触活动会导致突触AMPA受体减少以及mEPSC幅度下降。这种突触重塑的时间进程缓慢，类似于神经元AMPA受体的代谢半衰期。此外，抑制兴奋性突触传递会显著延长AMPA受体亚基GluR1的半衰期，这表明突触活动通过调节突触后AMPA受体的更新来调节mEPSC的大小。
