The glucocorticoid (GC)–cortisol receptor (GCR)–11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) system is involved in the regulation of Leydig cell function and spermatogenesis in mature animals. Herein, we describe the expression of the GCR and 11β-HSD2 and the occurrence of apoptosis during fetal development. Male fetuses were collected from Weeks 6, 10, 13, and 15 of pregnancy and from neonates. The testes were used for the immunocytochemical staining of GCR, 11β-HSD2 and for terminal deoxyribonucleotidyl transferase-mediated dUTP–digoxigenin nick end-labelling (TUNEL) staining of apoptosis. Apoptosis did not occur in any Leydig cells, but approximately 30% expressed GCR and 11β-HSD2. The number of GCR-positive cells was similar at all stages, but the number of 11β-HSD2-positive cells tended to be higher at Weeks 6 and 15. Steroid synthesis was also higher compared with Weeks 10 and 13. Apoptosis occurred in only a few germ cells. Nearly all germ cells were GCR positive at Weeks 10 and 13, when 11β-HSD2 was also increased. The total number of 11β-HSD2-positive germ cells was approximately 30%. Thus, elevated GCR expression coincided with the differentiation of gonocytes to spermatogonia and their migration to the basal lamina.