Correction for “Stress dynamically regulates behavior and glutamatergic gene expression in hippocampus by opening a window of epigenetic plasticity” by Carla Nasca, Danielle Zelli, Benedetta Bigio, Sonia Piccinin, Sergio Scaccianoce, Robert Nisticò, and Bruce S. McEwen, which was first published November 16, 2015; 10.1073/pnas.1516016112 (Proc. Natl. Acad. Sci. U.S.A. 112, 14960–14965).
The authors note, “An editing error occurred when assembling Fig. 1E. An enlarged image of the CA3 control area was inadvertently included as the CRS image for CA3 hippocampus. We have located the original images and have corrected the figure. The revised figure appears below.
Additionally, the acronym BDNF should have been spelled out as ‘brain-derived neurotrophic factor’ in the abstract.”
The published paper has been updated.
Differential responses of the hippocampus to novel and familiar stressors in chronically stressed mice. (A and B) The 21-d CRS decreased the transcription of presynaptic mGlu2 receptors, inhibitors of synaptic glutamate release, and resulted in a nonsignificant decrease in the transcription of the obligatory subunit NR1 of NMDA receptors in hippocampus. Two hours after AFS in CRS mice, mGlu2 transcripts were still down-regulated whereas hippocampal NR1/NMDA transcripts were significantly up-regulated. Conversely, 2 h after a known ARS in CRS mice, we observed no significant change in NR1/NMDA mRNA levels, but the CRS-induced decrease in mGlu2 in hippocampus was temporarily reversed [mGlu2, F3,20 = 9.75, P < 0.001 (stress); NR1/NMDA, F3,14 = 15.2, P < 0.001 (stress)]. (C) Immunohistochemistry analyses for mGlu2 expression in the subregions of the hippocampal formation (DG, CA3, and CA1) showed a subregional localization of CRS effects within the DG: CRS induced a large decrease in mGlu2 immunoreactivity in the DG, with no change in the CA3 and CA1. However, 2 h after a known ARS in CRS mice, the CRS-induced decrease in mGlu2 expression was temporarily reversed in the DG hippocampus, with no change in the CA3 and CA1 hippocampus. Conversely, 2 h after an unknown AFS in CRS mice, mGlu2 expression was still down-regulated in the DG, with no change in the CA3 and CA1 hippocampus [mGlu2, DG, F3,71 = 5.22, P < 0.01 (stress); CA3, F3,66 = 1.26; CA1, F3,65 = 1.67)]. (D) No significant change was observed, after CRS, in NMDA immunoreactivity within the hippocampal subregions (DG, CA3, and CA1). Two hours after a known ARS in CRS mice, we observed no significant change in NMDA expression within the hippocampal subregions whereas, 2 h after an unknown AFS in CRS mice, NMDA expression was increased in the DG, CA3, and CA1 hippocampus [NMDA, DG, F3,35 = 4.82, P < 0.01 (stress); CA3, F3,35 = 6.03, P < 0.01; CA1, F3,30 = 6.29, P < 0.01]. (E) Representative 10× images of hippocampal sections of NMDA immunoreactivity from unstressed mice (Top Left), CRS mice (Top Right), 2 h after ARS in CRS mice (Bottom Left) and 2 h after AFS in CRS mice (Bottom Right). Bars represent mean + SEM, and * indicates significant comparisons with corresponding controls, *P < 0.05, **P < 0.01.