Hypothalamic Protein Synthesis Essential for the Activation of the Lordosis Reflex in the Female Rat*

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Abstract
A discontinuous exposure to estradiol (E2) in two l-h segments is sufficient to activate progesterone-facilitated feminine sexual behavior in the rat at 24 h, provided that the second l-h segment of E2 treatment begins not fewer than 4 or more than 13 h after the end of the first segment of E2 treatment (sufficient treatment). In this study, the protein synthesis inhibitor anisomycin (ANI) was used to elucidate the time course of the changes in protein synthesis after sufficient treatment which are essential for the activation of the lordosis reflex in the female rat. If ANI (100/mg kg) was administered 15 min before the first segment, 15 min before the second segment, or between the two 1-h segments of E2 treatment, little or no sexual receptivity was observed at 24 h. However, if ANI was delayed until 2 or 6 h after the end of the second period of E2 treatment (0–1 h and 8–9 h), no significant decrease in the lordosis quotient or lordosis quality score was observed at 24 h. These data indicate that a large portion of the protein synthesis essential for the activation of the lordosis reflex is completed within 2 h after termination of sufficient treatment (in this particular paradigm, by 11 h after the initiation of E2 treatment). In separate experiments, three different doses of ANI (100, 30, and 10 mg/kg) were administered at various times relative to sufficient treatment in order to determine the magnitude and duration of protein synthesis inhibition in the mediobasal-hypothalamus preoptic (MBH-POA) which is able to abolish the activation of sexual receptivity. Inhibition of protein synthesis by approximately 60% in the MBH-POA for the 1-h duration of either segment of E2 treatment was sufficient to decrease significantly, but not abolish, sexual receptivity at 24 h (10 mg/kg ANI). To abolish sexual receptivity at 24 h, protein synthesis had to be inhibited by at least 40–80% in the MBH-POA for 2 consecutive h, both during and 1 h after the termination of either segment of E2 treatment (30 and 100 mg/kg ANI). Our data are consistent with the hypothesis that E2 activates the lordosis reflex, at least in part, by altering protein synthesis in the hypothalamus. The degree and magnitude of protein synthesis inhibition are quantitatively related to the frequency and strength of lordosis. Substantial interference with hypothalamic protein synthesis 2 or more h after the termination of sufficient treatment does not interfere with the expression of sexual receptivity at 24 h.