First published June 2, 2014 - More info
Stressful events during early childhood can have a profound lifelong influence on emotional and cognitive behaviors. However, the mechanisms by which stress affects neonatal brain circuit formation are poorly understood. Here, we show that neonatal social isolation disrupts molecular, cellular, and circuit developmental processes, leading to behavioral dysfunction. Neonatal isolation prevented long-term potentiation and experience-dependent synaptic trafficking of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptors normally occurring during circuit formation in the rodent barrel cortex. This inhibition of AMPA receptor trafficking was mediated by an increase of the stress glucocorticoid hormone and was associated with reduced calcium/calmodulin-dependent protein kinase type II (CaMKII) signaling, resulting in attenuated whisker sensitivity at the cortex. These effects led to defects in whisker-dependent behavior in juvenile animals. These results indicate that neonatal social isolation alters neuronal plasticity mechanisms and perturbs the initial establishment of a normal cortical circuit, which potentially explains the long-lasting behavioral effects of neonatal stress.
Tomoyuki Miyazaki, Kenkichi Takase, Waki Nakajima, Hirobumi Tada, Daisuke Ohya, Akane Sano, Takahisa Goto, Hajime Hirase, Roberto Malinow, Takuya Takahashi
Original citation: J. Clin. Invest. 2012;122(7):2690–2701. doi:10.1172/JCI63060.
Citation for this corrigendum: J. Clin. Invest. 2014;124(6):2807. doi:10.1172/JCI76901.
During the preparation of this manuscript, raw Western blotting data were inadvertently not included in the Supplemental material file, and a sentence referring to that data was not included at the end of the Figure 4 legend and also at the end of the Supplemental Figure 1 legend. The data have been added to the Supplemental material as Supplemental Figure 7, and the correct sentence is below.
See also Supplemental Figure 7.
The authors regret the error.