In freshwater eels held under conditions of captivity, puberty does not occur and gametogenesis is arrested at a very early developmental stage (early Type B spermatogonia only¹ ). To override this arrest, which has been attributed to gonadotropin insufficiency² , hCG has long been the treatment of choice; this treatment, whether as a single or repeated application, induces rapid spermatogonial proliferation and gonad growth³ . Despite the routine use of hCG for induction of testicular growth in eels for over 60 years, a robust dose-response experiment is essentially lacking. In this study, we therefore adopted a dose-response experimental design (single injection of 0 - 4,000 U hCG per fish of ~ 150 g) and compared two routes of administration (intramuscular and intraperitoneal) to obtain ED50 values around relative testicular weight (expressed as % of body weight). Spermatogonial proliferation was histologically discernable after 4 weeks with as little as 20 U, evidenced by the increased abundance of late Type B spermatogonia; however, relative testicular size was not different from the control group until at least 40 U was administered. Effects appeared to be associated with binding of hCG to LH-receptors on both Sertoli and Leydig cells. Interestingly, intramuscular injection of hCG was much more effective than intraperitoneal injection, preliminary analyses indicating that the ED50 for the former treatment equates to approximate 150 U/fish. The implications of hCG dose on sperm motility are currently assessed.