Fig. 5. Thinning of Pcdh- mutant retina reflects increased apoptosis during a restricted postnatal period. (A-F) Nuclear labeling of Pcdh-^del/del, Pcdh- ^fcon3/fcon3, and control retinas at E18.5 (A,B), P7 (C,D) and P15.0 (E,F). Mutant and control retinas are indistinguishable at E18.5 but INL and IPL are thinner in mutant retinas than in controls by P7. Although the INL becomes thinner in both mutants and controls over the subsequent 5 months, the difference between them is not progressive. (G,H) Thickness of NBL/INL (NBL at P0 and P3, INL at later stages) and IPL in control (black) and Chx10-Cre;Pcdh- ^fcon3/fcon3 mutant retina sections (red). The mutant NBL/INL and IPL develop normally through P3, then decline in thickness relative to controls over the next few weeks. Graphs show mean±s.e.m. from three or four animals. ^***P<0.001, Student's t-test. (I) NBL/INL and IPL thickness in Pcdh- ^fcon3/fcon mutant retinas, expressed as percentage of control. (J,K) Increased numbers of apoptotic cells, marked by cleaved caspase 3 immunoreactivity (red), in Pcdh- ^fcon3/fcon3 mutant retinas at P7 compared with controls. (L,M) Quantification of cleaved caspase 3 immunopositive cells in control (black) and Pcdh- ^fcon3/fcon3 mutant (red) retinas. Differences between genotypes are significant in the NBL/IPL at P0 and P7, but in the ganglion cell layer only at P7. Results from three to six animals per stage. ^***P<0.001; ^**P<0.01; ^*P<0.05; Student's t-test or Mann-Whitney test. Abbreviations as in Fig. 1. Scale bars: 20 µm.