NEURAL BASIS OF DIURNAL PERIODICITY IN RELEASE OF OVULATION-INDUCING HORMONE IN FOWL

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Abstract
White Leghorns, Rhode Island Reds, and crosses between these breeds were individually caged in laying batteries, under electric lights from 6 a.m. through 8 p.m. with access to feed and water at all times. The usual records of lay at hourly intervals from 8 a.m. through 4 p.m. served as the basis of selecting experimental hens. The 1st, or C1, ovulation was estimated to occur at 6 a.m., the 2d, or C2, ovulation at 1030 a.m. of the following day. The C1 ovulation of the next sequence (series of ovulations occurring on consecutive days) occurred 43.5 hours after the C2 ovulation of the preceding sequence. Based on these relationships estradiol benzoate dissolved in corn oil (5 mg/ml) was injected at levels of 1-2.5 mg/hen 14-41 hours before the expected C1 ovulation and 11-28 hours before the expected C2 ovulation. The occurrence of normal or suppressed ovulation was determined by palpation for presence or absence of the ovidcual egg. If suppressed, palpation was timed to give approximate information on the hour of the delayed ovulation. The reliability of the palpation method was checked by autopsy on 9 hens 12-14 hours after the occurrence of C2 ovulations delayed for one day, or 60 hours after administering estradiol benzoate. The ovaries of these hens were normal, indicating that the estrogen was not causing selective atresia of the next ovulable follicle. 5-10% of the hens selected for C1 ovulation were found to fail to ovulate, and failure of C2 ovulation was less frequent, but these deviations should be considered in interpreting the results. Of 88 hens injected with estradiol benzoate before the expected C1 ovulation, 12 or 14% had suppressed ovulations, and of these, 8 or 67% were delayed by only one day. All delayed C1 ovulations occurred at or close to the hour of the expected C1 ovulations, i.e, a delay of 24 hours or some multiple of 24 hours. Of 119 hens treated before the expected C2 ovulation, 66 or 55% had suppressed ovulations. 45% of these were delayed by only one day, and occurred at 6 a.m. after a delay of 19-20 hours. The effect of estradiol benzoate in suppressing C1 or C2 ovulations was independent of the time from injection to normally expected ovulation. Estradiol depropionate and diethylstilbestrol had the same effect as estradiol benzoate in suppressing ovulation. These studies suggest that suppression of ovulation is due to decreased excitability of the postulated neural component of the OIH (ovulation-inducing hormone) release mechanism during the relatively limited hours of normally high excitability. The observation that ovulation, following suppression, occurred during the hours of the 24 when it normally took place, indicated that the neural mechanism exhibited diurnal periodicity in its thresholds of response to excitation hormones. Results of this study are compared with those obtained with rats and ring doves.