Posterior Hypothalamic Lesions Advance the Onset of Puberty in the Female Rhesus Monkey*

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Abstract
The effects of experimental lesions in the posterior hypothalamus and the anterior hypothalamus on menarche and 1st ovulation were examined in nonhuman primates. With the aid of X-ray ventriculography, bilateral lesions were made by passing a radiofrequency current through a thermister electrode in the posterior hypothalamus (n = 7) or the anterior hypothalamus (n = 6) of female rhesus monkeys at 18 mo. of age. Four animals that received sham lesions as well as 4 normal females of a similar age served as controls. All animals were caged individually and examined daily for vaginal bleeding and sex skin color change. Developmental changes in gonadotropins, ovarian steroids, body weight and nipple size were monitored throughout the experiments. The time of 1st ovulation was determined by laparoscopic observation of the newly formed corpus luteum and by the level of circulating progesterone. Histological examination confirmed that the bilateral lesions in the hypothalamus were approximately 2-3 mm in diameter and overlapped midline. Primary sites of posterior hypothalamic lesions included the premamillary area and the posterior nucleus, while the infundibular nucleus and the median eminence were entirely spared. The posterior lesions encroached upon the mamillary nuclei caudally in most cases and upon the ventromedial nucleus rostrally in some cases. Primary sites of anterior hypothalamic lesions included the medial preoptic area, the periventricular preoptic nucleus and the anterior hypothalamic nucleus. Partial lesions of the diagonal bundle of Broca, the medial preoptic nucleus and the paraventricular nucleus were also detected. Posterior hypothalamic lesions advanced the ages at menarche (22.2 .+-. 1.3 mo.; P < 0.001) and 1st ovulation (40.7 .+-. 2.7 mo.; P < 0.05) compared to those of control animals (menarche, 30.3 .+-. 3.1; 1st ovulation, 51.2 .+-. 3.3 mo.). The body weight at menarche of these lesioned animals (2.62 .+-. 0.11 kg) was smaller (P < 0.05) than that of controls (3.14 .+-. 0.20 kg), but the body weight at 1st ovulation of lesioned animals (4.36 .+-. 0.28 kg) was not different from that of controls (4.57 .+-. 0.13 kg). Hormonal and physical changes during maturation, i.e., an increase in circulating estradiol and growth in nipple size before menarche and 1st ovulation, occurred earlier in the lesioned animals and the growth spurt before 1st ovulation not only began earlier but also attained mature levels several months earlier than that in control animals. In contrast, anterior hypothalamic lesions did not induce consistent effects on the onset of puberty. In general, animals with anterior hypothalamic lesions had poor health. Although 3 of 6 animals, which did not have health problems, had an earlier menarche (23.2 .+-. 2.5 mo.) and 1st ovulation (49.9 .+-. 7.1 mo.), some of them had delayed menarche and 1st ovulation, and some died before menarche and/or 1st ovulation. Lesions in the posterior hypothalamus induced true precocious puberty, but further study is needed to determine the effect of anterior hypothalamic lesions.