Fig. 5.

Mutations of the RA synthesizing Raldh1 and Raldh3 genes, as well as global reductions in vitamin A supply, decrease numbers of GABAergic interneurons in the cortex. (a) The density of parvalbuminpositive cells was not influenced by the Raldh mutations, but (b) calbindin-expressing cells were diminished in the homozygous Raldh1 null mutants, and (c) density of calretinin-positive cells were reduced in both the Raldh1 null mutants and Raldh3-heterozygous null mutants (density = number of cells per 300 mm², *control vs. Raldh1−/− t = 3.01, p < 0.02, **control vs. Raldh3−/− t = 2.47, p < 0.03). Panels (d) and (e) show data from adult retinol-binding protein (RBP) mutants, which were exposed in addition to a vitamin A-deficient (VAD) diet during the entire time of cortex development. In these mice (Rbp4−/−, VAD) (d) the parvalbumin-positive cells were only marginally affected, but (e) calbindin-labelled cells were reduced to almost half their normal counts (density = number of cells per 300 mm², *control vs. Rbp4−/−, VAD t = 11.12, p < 0.0001).