In a study, males over 14 months old showed active spermatogenesis.

The spermatogenesis is less efficient at lower and higher temperatures.

Spermatogenesis takes place within several structures of the male reproductive system.

It is also considered likely to cause inhibition of spermatogenesis.

The testes grow in response to the start of spermatogenesis.

Mouse studies suggested an essential role of this protein in spermatogenesis.

In males, testes are often small, but spermatogenesis is thought to be normal.

Therefore, once spermatogenesis has begun, no more Sertoli cells are created.

Some pubertal male patients will have impaired spermatogenesis before they begin therapy.

Further analysis showed spermatogenesis had arrested in these mice.

His research focused on the hormonal control of spermatogenesis.

The process of spermatogenesis is highly sensitive to fluctuations in the environment, particularly hormones and temperature.

The first occurs inside the Wolbachia infected male during spermatogenesis and is called modification.

Spermatogenesis most likely occurs after the emergence from hibernation.

The developing male germ cells do not complete cytokinesis during spermatogenesis.

Testosterone is required for normal spermatogenesis and inhibits the hypothalamus.

It is the female form of gametogenesis; the male equivalent is spermatogenesis.

However, it fills the purpose as the female counterpart of the male spermatid in spermatogenesis.

Oogenesis and spermatogenesis have many features in common, they both involve:

The Sertoli cells themselves mediate parts of spermatogenesis through hormone production.

Its predominant expression in testes suggests a role in spermatogenesis.

Inhibin B may be used as a marker of spermatogenesis function and male infertility.

The intratesticular testosterone is necessary for spermatogenesis from the sertoli cells.

Male B. nicefori are capable of sexual activity year round, continually undergoing spermatogenesis.