Differential testosterone secretory capacity of the testes of aggressive and nonaggressive house mice during ontogeny

Abstract

In this study, testosterone secretory capacity of testicular Leydig cells during ontogeny was determined in males of an aggressive and a nonaggressive genetic selection line of wild house mice. Neonates, 23‐day‐old prepubertals, and adult male mice were studied. A morphometric method was used to quantify 3β‐hydroxy steroid dehydrogenase (3β‐3HSD)‐stained Leydig cells in testicular sections to determine testosterone secretory capacity. We consider this parameter to reflect circulating testosterone in the plasma. The results of this study show that the testosterone secretory capacity of Leydig cells in the testis changes differentially during development in males of the aggressive and nonaggressive selection lines. This capacity is highest in the aggressive selection line males at adulthood and at the prepubertal age of 23 days. Surprisingly, at birth, the highest T‐secretory capacity was observed in the males of the nonaggressive selection line. The significance of an interaction between genetic factors and differences in perinatal testosterone for the individual variation in adult aggressive behavior is discussed.

Brain aromatase activity and plasma testosterone levels are elevated in aggressive male mice during early ontogeny

“…In adulthood these selection lines differ in several T-related parameters. Thus, males of the aggressive short attack latency (SAL) line have higher plasma T levels, higher seminal vesicle weights [49], and larger testicular Leydig cell percentages [13], as compared to males of the non-aggressive long attack latency line (LAL). Although T is reported to induce AA in the adult dove [20][21][22] and rat brain [35,44], the aggressive SAL males show lower levels of aromatase activity (AA) in the preoptic area (POA) of the brain, despite higher circulating T [8].…”

Aromatase activity in the preoptic area differs between aggressive and nonaggressive male house mice

“…The higher POA AA indicates a higher estradiol formation in the POA of nonaggressive LAL males than in aggressive SAL males, assuming that the aromatase substrate T is equally available in brains of both selection lines. However, we have shown in previous studies that adult nonaggressive LAL males have a lower plasma T level (SAL: 6.3 + 0.6 and LAL: 4.8 2 0.4 @ml plasma), a lower seminal vesicle weight (55), and a smaller percentage of testicular Leydig cells (SAL: 4.25% and LAL: 3.0%) (17), as compared to aggressive SAL mice. Accordingly, high levels of circulating T are not necessarily positively correlated with brain AA.…”

“…The males of these strains not only differ in aggression, but also in several Trelated parameters. Adult males of the aggressive short attack latency (SAL) line have a higher plasma T level, a higher seminal vesicle weight (.55), and a larger testicular T production capacity (17), as compared to nonaggressive males of the long attack latency (LAL) line. Moreover, aromatase activity occurs in androgen target areas of the mouse brain (61).…”

Genetic differences in female house mice in aggressive response to sex steroid hormone treatment

“…Furthermore, prepubertally castrated SAL males show a higher aggressive response following adult T replacement than similarly treated LAL animals, suggesting a higher T sensitivity of the central nervous system (32). However, neonatally the LAL males have a larger testicular T production capacity than SAL males at the same age (10). Moreover, after neonatal testosterone treatment, LAL males showed a further reduction in aggressive behavior at adult age, whereas aggression of SAL males was not affected (9).…”