Recovery of lordotic activity by dorsal deafferentation of the preoptic area in male and androgenized female rats

Yasuhiko Kondo, Akira Shinoda, Korehito Yamanouchi, Yasumasa Arai
In: Physiology & Behavior · 1986 · vol. 37(3) , pp. 495–498 · doi:10.1016/0031-9384(86)90212-x · PMID:3749307 · W1997419976
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Dorsal deafferentation of the preoptic area restored lordotic activity in castrated male and androgenized female rats, with reduced responsiveness in androgenized females correlating negatively with neonatal testosterone dose.

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Abstract

Lordotic activity was examined in male and neonatally androgenized female rats following dorsal deafferentation of the preoptic area (POA). Female pups were injected with various doses (100, 250, 500, or 1000 micrograms) of testosterone propionate (TP) on day 3 postpartum. Ten weeks after birth, all animals were castrated, then half of the castrated males and females in each group were subjected to dorsal deafferentation of the POA (anterior roof deafferentation: ARD) by using an L-shaped Halász knife in order to transect the dorsal forebrain efferents which are thought to exert an inhibitory influence on the lordosis mediating mechanism. Animals were implanted subcutaneously with Silastic tubes containing estradiol-17 beta (E2). Observations of lordosis behavior were carried out 5, 10, and 15 days after implantation of E2. Three to six hours before each behavioral test, all rats were injected with 0.5 mg progesterone. Regardless of the dose of TP given neonatally, androgenized females, as well as males, showed low levels of lordotic behavior. In contrast, males with ARD and androgenized females with ARD displayed lordosis more frequently than males without ARD, and androgenized females without ARD. Lordotic activity in the androgenized females with ARD was negatively correlated with the dose of TP given neonatally. The ARD females injected with a large dose (1000 micrograms) of TP neonatally were significantly less receptive than those injected with lower doses of TP and ARD males. These results suggest that a large dose of neonatal TP may cause permanent changes in not only the neural substrates for lordosis inhibition affected by ARD but also other structures involved in lordosis facilitation.

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