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In our recent paper (Miyashita et al., 2013), we showed that long-term, highlevel channelrhodopsin-2 (ChR2) expression by in utero electroporation (IUE) produces structural abnormalities in the axons of ChR2-expressing pyramidal cells in rat somatosensory cortex. In the Discussion of our paper, we mentioned that such abnormalities were not observed in an earlier study using long-term IUE of ChR2 under the same promoter (Huber et al., 2008). A methodological difference has been brought to our attention that likely explains this difference. Huber et al. expressed wildtype ChR2 (Chop2-315 from Nagel et al., 2003), while we expressed hChR2 that was codonoptimized for higher mammalian expression (Zhang et al., 2006). This suggests that lower ChR2 protein levels in the Huber study may have enabled long-term expression without axonal malformations. This further supports our main conclusion that morphological abnormalities are associated with high-level, long-term expression of ChR2 protein, and that lower level expression is necessary for long-term studies.