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XB-ART-55130
Nat Commun January 1, 2018; 9 (1): 2893.

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

He HY , Shen W , Zheng L , Guo X , Cline HT .


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.

PubMed ID: 30042473
PMC ID: PMC6057951
Article link: Nat Commun
Grant support: [+]

Species referenced: Xenopus
Genes referenced: dlg4 erf gria1 gria2 rho srf


Article Images: [+] show captions
References [+] :
Aizenman, Visually driven modulation of glutamatergic synaptic transmission is mediated by the regulation of intracellular polyamines. 2002, Pubmed, Xenbase