Figure 3. GLE delayed rhodopsin-IR, but not recoverin-IR, in developing retinas (PN5-PN60). The developing retinas at PN5-PN60 from (A–L) the control and (M–X) GLE mice were double labeled with antibodies against rhodopsin (red: A–D and M–P) and recoverin (green: E–H and Q–T), and colabeling was examined in merged images (yellow: I–L and U–X). In the control retinas at (A, E, and I) PN5 and (B, F, and J) PN7, the ISs, ONL, and OPL were colabeled with rhodopsin and recoverin, which increased at PN7. C, G, and K: At PN10, the OS expressed rhodopsin-IR, and extensive colabeling with recoverin occurred in the ISs, ONL, and OPL. D, H, and L: In young adult control retinas (PN60), the OSs were intensely rhodopsin-IR, and there was extensive labeling in the ISs, ONL, and OPL. In the distal OPL, the smaller rod spherules [24] were colabeled (yellow pixels), whereas the larger cone pedicles in the proximal OPL [24] were only recoverin-IR (green pixels). In the GLE retinas at (M, Q, and U) PN5 and (N, R, and V) PN7, the ISs, ONL, and OPL were rhodopsin-IR and recoverin-IR, and an increased amount of colabeling was seen in all the layers. Relative to the age-matched controls, the ONL thickness increased. O, S, and W: At PN10, OSs were rhodopsin-IR, and extensive colabeling with recoverin occurred in the ISs, ONL, and OPL. Relative to the age-matched controls, the ONL thickness increased. P, T, and X: In the PN60 GLE retinas, the OSs, ONL, and OPL were intensely rhodopsin-IR and almost completely colabeled with recoverin. Relative to the age-matched controls, the ONL and OPL thickness increased, and the number of rod spherules increased as described [21]. Scale bar = 40 μm. GLE = Gestational lead exposure; IR = immunoreactivity; PN = postnatal; IS = inner segment; OS = outer segment; ONL = outer nuclear layer; OPL = outer plexiform layer.