Gap Junctions in A8 Amacrine Cells Are Made of Connexin36 but Are Differently Regulated Than Gap Junctions in AII Amacrine Cells
- 1Animal Navigation/Neurosensorics, Institute for Biology and Environmental Sciences, University of Oldenburg, Oldenburg, Germany
- 2Research Center Neurosensory Science, University of Oldenburg, Oldenburg, Germany
A Corrigendum on
Gap Junctions in A8 Amacrine Cells Are Made of Connexin36 but Are Differently Regulated Than Gap Junctions in AII Amacrine Cells
by Yadav, S. C., Tetenborg, S., and Dedek, K. (2019). Front. Mol. Neurosci. 12:99. doi: 10.3389/fnmol.2019.00099
In the original article, there was a mistake in Figure 5 as published. The line scans in Figures 5E,F depicting the channel intensity of the respective ROIs in Figures 5B,C, were swapped by mistake. The corrected Figure 5 appears below.
Figure 5. Co-localization of A8 gap junctions with bipolar cell terminals in vertical sections. (A–C) Single retinal slices of Ier5-EGFP (A8 cell) mouse stained with Cx36 and bipolar cell markers: VGluT1 (A), secretagogin [(B), SCGN], and synaptotagmin-2 [(C), Syt2]. Square white boxes in (A–C) are the selected ROIs shown in (A'–C””). Arrows denote co-localization of all the three channels which is also represented in the normalized intensity plots (D–F). (D–F) Intensity plot for three channels, corresponding to (A–C). The respective inset represents the single scan overlay of the three channels. The plot denotes normalized pixel intensity of three channels in y-axis, and the x-axis represents the relative distance of peak intensities of the three individual channels. Scale bar: (A–C), 10 μm; (A'–C””), 2.5 μm.
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Keywords: amacrine cell, bipolar cell, gap junction, electrical synapse, connexin36, retina, dopamine
Citation: Yadav SC, Tetenborg S and Dedek K (2019) Corrigendum: Gap Junctions in A8 Amacrine Cells Are Made of Connexin36 but Are Differently Regulated Than Gap Junctions in AII Amacrine Cells. Front. Mol. Neurosci. 12:149. doi: 10.3389/fnmol.2019.00149
Received: 10 May 2019; Accepted: 24 May 2019;
Published: 12 June 2019.
Edited and reviewed by: Volker Eulenburg, University Hospital Leipzig, Germany
Copyright © 2019 Yadav, Tetenborg and Dedek. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Karin Dedek, a2FyaW4uZGVkZWsmI3gwMDA0MDt1bmktb2xkZW5idXJnLmRl