Abstract
Unilateral compensatory hypertrophy of the gonad after hemicastration has been extensively studied in males and females (reviews by Grant, 1956; Edgren, Parlow, Peterson & Jones, 1965; McClaren, 1966; Peppler, 1969). The mechanisms responsible for the compensatory growth are, however, as yet, undefined. One theory suggests that the loss of a gonad results in a decrease in circulating steroids which reduces their negative feedback effect on the hypothalamic-hypophysial axis and consequently triggers an increased outflow of gonadotrophins. An alternative view is that the remaining gonad is stimulated by more gonadotrophin because of a decrease in the rate of utilization. With either of these possibilities the amount of circulating gonadotrophin should increase over the normal intact level. However, presently available bioassay techniques have not shown any changes in plasma or pituitary gonadotrophins in the hemiovariectomized female rat (Edgren et al. 1965; McClaren, 1966). Previous experiments with parabionts (Johnson, 1966) indicated that unilateral

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