Role of a Uterine-Placental Factor in the Cessation of the Semicircadian Rhythm of Tuberoinfundibular Dopaminergic Neuronal Activity at Midpregnancy in the Rat

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Abstract
During early pregnancy in the rat, the secretion of prolactin exhibits daily surges which appear to be related temporally to changes in the activity of tuberoinfundibular dopaminergic (TIDA) neurons. The present study was undertaken to determine:(1) the temporal relationships between the cessation of the prolactin surges at midpregnancy and the termination of the semicircadian pattern of TIDA neuronal activity, and (2) if the uterine-placental unit is required for the cessation of these patterns. TIDA neuronal activity was estimated from the rate of dopamine synthesis in the median eminence, which was measured in vivo by determining the rate of DOPA accumulation after the administration of an inhibitor of aromatic L-amino acid decarboxylase. Nocturnal surges of prolactin occurred on days 6–11 of pregnancy but not on days 12 and 13, while diurnal surges occurred on days 6–9. TIDA neurons exhibited a biphasic pattern of activity on days 8–10 of pregnancy with activity being significantly lower at 04.30 h than at 12.00 h. On days 11–13 of pregnancy, this pattern was lost and activity was constantly maintained at the higher values. Nocturnal surges of prolactin that normally cease after day 11 of pregnancy were still observed on days 12 and 13 if the pregnant rats were hysterectomized on day 6. Furthermore, the biphasic pattern of TIDA neuronal activity persisted until day 13 if pregnant rats were hysterectomized on day 6. The administration of bromocriptine, a dopaminergic agonist which in nonpregnant female rats reduces TIDA neuronal activity by virtue of its ability to reduce circulating concentrations of prolactin, reduced TIDA neuronal activity in 6-day pregnant animals, but was ineffective in 13-day pregnant rats. Bromocriptine was, however, able to reduce the activity of TIDA neurons on day 13 if the pregnant rats had been hysterectomized on day 6. These results suggest that at midpregnancy a uterine-placental factor takes over from prolactin in stimulating TIDA neurons; this factor appears to be responsible for terminating the semicircadian pattern of prolactin secretion.