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Fig. 1. Neuroanatomy of megalin-deficient neonates and embryos. (A,B) External
appearance of wild-type (A) and megalin–/– neonates
(B), highlighting craniofacial abnormalities in the receptor-deficient mouse.
(C,D) Coronal H+E stained sections through the rostral brain of E18.5 embryos,
depicting enlarged ventricles in the megalin-deficient animal (D) compared
with the control (C). (E,F) Horizontal sections through the brain at E18.5,
demonstrating a single cerebral hemisphere with a central fused ventricle in
the megalin–/– embryo (F) compared with
bilateral hemispheres with two lateral ventricles in the control (E). (G-I)
Coronal forebrain sections of wild-type (G) and
megalin–/– E14.5 embryos (H,I), with abnormalities
ranging from enlarged ventricles (H) to exencephalus and a common ventricular
system (I). (K-N) Sagittal forebrain sections from wild type (K,L) and
megalin-deficient E12.5 embryos (M,N) subjected to H+E staining (K,M) or
detection of cell death by TUNEL assay (L,N).
megalin–/– embryos suffer from a reduction in
neuroepithelial wall thickness (M, arrowhead) compared with controls (K) that
coincides with massive apoptosis in the roof of the cerebral cortex (N,
arrowhead). (O,P) Lateral aspects of wild-type (O) and
megalin–/– (P) E10.5 embryos. Note the reduced size of
the telencephalic vesicles in the knockout. (Q,R) Coronal forebrain sections,
indicating a decrease in thickness of the ventral neuroepithelium that is most
pronounced in the AEP and the MGE of megalin–/– embryos
(R) compared with megalin+/+ embryos (Q). (C-M,O-R: H+E staining).
AEP, anterior entopeduncular area; MGE, medial ganglionic eminence; tv,
telencephalic vesicles.
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