Differential Alterations in Dopamine Turnover Rates in the Stalk-Median Eminence and Posterior Pituitary during the Preovulatory Prolactin Surge

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Abstract
The relative contributions of dopamine (DA) and prolactin-releasing factor (PRF) in generating the prevolutionary prolactin (PRL) surge were investigated. Immature female rats were injected with pregnant mare''s serum gonadotropin (PMSG) on day 28. Jugular blood was collected hourly on days 30 and 31. PRL levels were low in the morning of day 30, rose 10-12 times to peak levels from 14.00 to 16.00 h, reached a prolonged plateau form 18.00 to 24.00 h, and reduced to basal levels in the morning of day 31. All PMSG-treated rats ovulated an average of 13014 ova. PRL levels in age-matched control rats were low throughout this time, and no oviductal ova were present. DA turnover rates in the stalk-median eminence (SME) and posterior pituitary (PP) were determined from the decline in tissue DA after injecting .alpha.-methyl=p-tyrosine (.alpha.-MPT), a competitive inhibitor of tyrosine hydroxylase. DA turnover rates increased or were unaltered in the SME and PP, respectively, during the peak PRL phase as compared to presurge rates. In contrast, DA turnover rates were significantly reduced in both tissues during the plateau phase. The turnover rate in the SME, but not the PP, was increased in the morning of day 31. DA turnover rates in control rates never changed. Injection of .alpha.-MPT to PMSG-treated rats increased PRL levels at all times examined except during the plateau phase. Blood PRL levels were also determined in PMSG-treated rats following posterior pituitary lobectomy or sham lobectomy. The PRL surge was similar in both groups and all rats ovulated. These data suggest that the peak PRL surge occurs in spite of high DA activity and the presence of DA input to the anterior pituitary, and is therfore sustained by a non-dopaminergic mechanism. The prolongation of the PRL surge likely results from the decreased activity of DA neurons in both the SME and PP and its termination is caused by increased DA activity in the SME only. There is no evidence for a PRF input from the PP during the preovulatory PRL surge in PMSG-treated rats, but a hypothalamic PRF might be involved.