Neonatal Leydig Cells

Just after birth, the number of Leydig cells again increases to a peak at 2 to 3 mo of age, contributing to a second surge in plasma testosterone levels. At this stage, Leydig cells contain abundant SER membranes and mitochondria, as well as varying amounts of lipid droplets (4,24-27). In the neonatal testis, fetal Leydig cells persist through at least 3 mo after birth. Postnatal increase in the number of these cells most likely results from recruitment of interstitial precursor cells. After this increase, neonatal Leydig cell numbers regress rapidly to a nadir by the end of the first year. The neonatal period is relatively brief, extending only through the first year of life (28,29).

After the first year and continuing for a decade, Leydig cells are in a state of prepu-bertal quiescence. During this phase, well-differentiated Leydig cells are absent from the interstitial space. In their place are partially differentiated Leydig cells and primitive fibroblastic cells. At this stage, Leydig cells are dispersed in a loose connective tissue matrix and contain elongated nuclei with scarcely visible cytoplasm. It has been proposed that these partially differentiated Leydig cells and primitive fibroblasts are precursors of adult Leydig cells (13,25,30-32).

Time Line:

Fetal Birth Neonatal Prepubertal Adult Senescence -1<-/-/-----------ยป

Mesonephros

Mesenchymal cells

Neural crest?

FLC

NLC

ILC

ALC

Fig. 3. Human Leydig cell development. FLC, fetal Leydig cells; NLC, neonatal Leydig cells; ILC, immature Leydig cells; ALC, adult Leydig cells, P, fibroblastic precursors of Leydig cells. The cross-hatched circles indicate degeneration of FLC, NLC, and ALC. The far left-hand column of the compartments represents stem cells, including mesonephros-derived mesenchyme and/or neural crest. The time line shows the developmental period: fetal (from 8 wk gestation to birth), neonatal (first year of life), prepubertal (from second year to approx 10 yr of life), and adult (from approx 13 yr old onward). According to the hypothesized ontogeny, mesonephros-derived mesenchymal cells, or possibly neural crest, supply precursors for FLC. After birth, NLC arise from redifferentiation of FLC and new differentiation from mesenchymal cell precursors. After the first year of life, NLC regress to the partially differentiated ILC. ILC are then present through childhood. Starting at approx 10 yr of age, ILC and mesenchymal precursors again differentiate, maturing into ALC. With senescence, Leydig cells begin to lose full steroidogenic function and, as indicated, atrophy.

Fig. 3. Human Leydig cell development. FLC, fetal Leydig cells; NLC, neonatal Leydig cells; ILC, immature Leydig cells; ALC, adult Leydig cells, P, fibroblastic precursors of Leydig cells. The cross-hatched circles indicate degeneration of FLC, NLC, and ALC. The far left-hand column of the compartments represents stem cells, including mesonephros-derived mesenchyme and/or neural crest. The time line shows the developmental period: fetal (from 8 wk gestation to birth), neonatal (first year of life), prepubertal (from second year to approx 10 yr of life), and adult (from approx 13 yr old onward). According to the hypothesized ontogeny, mesonephros-derived mesenchymal cells, or possibly neural crest, supply precursors for FLC. After birth, NLC arise from redifferentiation of FLC and new differentiation from mesenchymal cell precursors. After the first year of life, NLC regress to the partially differentiated ILC. ILC are then present through childhood. Starting at approx 10 yr of age, ILC and mesenchymal precursors again differentiate, maturing into ALC. With senescence, Leydig cells begin to lose full steroidogenic function and, as indicated, atrophy.

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