At autopsy, the OE, bony septae, and contiguous cribriform plate were removed en bloc and fixed for 24 to 36 hours in 10% neutral-buffered formalin, decalcified for 14 to 16 days in distilled water with sodium EDTA, sodium hydroxide, and glycerol at pH 7.1 to 7.4.30,31 Tissue blocks were then cut into coronal blocks, dehydrated in graded ethanols to xylene isomers, and embedded in paraffin, as previously described.30 Ten-millimeter-thick serial sections were cut from a central block of olfactory tissue in each case. Three double immunohistochemical labeling procedures were conducted for each case, in duplicate, using antibodies: (1) Me20.4 (1:10 for p75NGFR32), (2) growth-associated protein GAP43 (1:1000, Sigma Chemical, St Louis, Mo33), and (3) olfactory marker protein (OMP; 1:200034). The p75NGFR antibody recognizes a receptor to trophic molecules and is selectively expressed in the dividing precursor basal cells of the OE.30,31 As basal cells commit to neuronal maturation, expression of p75NGFR ceases and the postmitotic immature neurons begin to express GAP43. As these attain a mature phenotype, they begin to express OMP and GAP43 diminishes.35,36 Slides were double labeled for p75NGFR/GAP43, p75NGFR/OMP, and GAP43/OMP. Immunohistochemistry studies were performed by the peroxidase-antiperoxidase method, and used 3′,3′-diaminobenzidine as previously described.30,37 In each instance, the 3′,3′-diaminobenzidine chromogen solution for the first antibody procedure included 2.5% nickel sulfate, while this was excluded for the second antibody. This yielded a black reaction product identifying the first antibody and brown for the second. All cases (schizophrenic and control samples), as well as positive and negative control slides (with and without primary antibody), were run simultaneously with precise timing of reactions for each double immunohistochemical run.