β-nerve growth factor participates in an auto/paracrine pathway of regulation of the meiotic differentiation of rat spermatocytes

NGF appears to be involved in spermatogenesis. However, mice lacking NGF or TrkA genes do not survive more than a few days whereas p75^NTR knockout mice are viable and fertile. Therefore, we addressed the effect of βNGF on spermatogenesis by using the systems of rat germ cell culture we established previously. βNGF did not modify the number of Sertoli cells, pachytene spermatocytes, secondary spermatocytes nor the half-life of round spermatids, but increased the number of secondary meiotic metaphases and decreased the number of round spermatids formed in vitro. These effects of βNGF were reversible and maximal at about 4 × 10^-11 M. Conversely, K252a, a Trk-specific kinase inhibitor, enhanced the number of round spermatids above that of control cultures. The presence of βNGF and its receptors TrkA and p75^NTR was investigated in testis sections, in Sertoli cell and germ cell fractions, and in germ cell and Sertoli cell co-cultures. βNGF was detected only in germ cells from pachytene spermatocytes of stages VII up to spermatids of stages IX-X. TrkA and p75 ^NTR were detected in Sertoli cells and in these germ cells. Taken together, these results indicate that βNGF should participate in an auto/paracrine pathway of regulation of the second meiotic division of rat spermatocytes in vivo.