Influences of neonatal gonadectomy or androgen exposure on the sexual differentiation of the rat ventromedial hypothalamus.

Antidromic action potentials were recorded extracellularly from 830 neurones in the ventromedial hypothalamus of 137 urethane‐anaesthetized rats following electrical stimulation of the central grey matter of the mesencephalon. Antidromic spike latency (range: 1.4‐45.0 ms) and stimulus threshold (85‐1800 microA) were determined for each response in twenty‐five normal males (n = 157) and thirty females ovariectomized as adults (n = 167) as well as in thirty‐six neonatally castrated males (n = 223) and forty‐six females neonatally treated with testosterone propionate (n = 283). Frequency distribution of the antidromic spike latency was multimodal in each group of animals, and was different between the groups. Significantly more of the cells had antidromic spike latencies within two ranges of 6.0‐11.0 ms and 14.0‐20.0 ms, respectively, in the ovariectomized females than in the normal males. The proportion of cells with longer latencies was modified by testosterone administration to females or castration of males during the early post‐natal period. Neuronal populations with shorter latencies withstood endocrine manipulations. Oestrogen administration to adults significantly decreased antidromic activation thresholds in ovariectomized females and neonatally castrated males. High threshold values in the testosterone‐treated, constant oestrous females did not change after ovariectomy as adults or oestrogen supplementation. It is concluded that sexual dimorphism exists in the hypothalamic neurones shown to project to the central grey and that difference depends at least partially on neonatal endocrine treatments.