Excitatory synaptic dysfunction cell-autonomously decreases inhibitory inputs and disrupts structural and functional plasticity

Hai-yan He, Wanhua Shen (), Lijun Zheng, Xia Guo and Hollis T. Cline ()
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Hai-yan He: The Scripps Research Institute
Wanhua Shen: College of Life and Environmental Sciences, Hangzhou Normal University
Lijun Zheng: College of Life and Environmental Sciences, Hangzhou Normal University
Xia Guo: College of Life and Environmental Sciences, Hangzhou Normal University
Hollis T. Cline: The Scripps Research Institute

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Functional circuit assembly is thought to require coordinated development of excitation and inhibition, but whether they are co-regulated cell-autonomously remains unclear. We investigate effects of decreased glutamatergic synaptic input on inhibitory synapses by expressing AMPAR subunit, GluA1 and GluA2, C-terminal peptides (GluA1CTP and GluA2CTP) in developing Xenopus tectal neurons. GluACTPs decrease excitatory synaptic inputs and cell-autonomously decreases inhibitory synaptic inputs in excitatory and inhibitory neurons. Visually evoked excitatory and inhibitory currents decrease proportionately, maintaining excitation/inhibition. GluACTPs affect dendrite structure and visual experience-dependent structural plasticity differently in excitatory and inhibitory neurons. Deficits in excitatory and inhibitory synaptic transmission and experience-dependent plasticity manifest in altered visual receptive field properties. Both visual avoidance behavior and learning-induced behavioral plasticity are impaired, suggesting that maintaining excitation/inhibition alone is insufficient to preserve circuit function. We demonstrate that excitatory synaptic dysfunction in individual neurons cell-autonomously decreases inhibitory inputs and disrupts neuronal and circuit plasticity, information processing and learning.

Date: 2018
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DOI: 10.1038/s41467-018-05125-4

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