Dehydration attenuates plasma prolactin response to suckling through a dopaminergic mechanism.

The tuberoinfundibular dopaminergic neurons projecting to the median eminence are well accepted as a major physiological regulator of adenohypophyseal PRL secretion. However, recent evidence has shown that dopamine (DA) in the neurointermediate lobe also has an inhibitory effect on PRL secretion by anterior pituitary. Since the neurointermediate is innervated by the tuberohypophyseal dopaminergic (THDA) neurons, which is known to be selectively activated by dehydration of the animal, the aim of this study was to investigate the physiological role of the THDA system in PRL release during lactation. On the day of the experiments, the litters were separated from the mothers for 4 h before initiation of the suckling stimulus. The suckling-induced PRL surge was detected on three consecutive days. On the first day the normal response was tested; then immediately after taking the last blood samples, drinking solutions were changed to the high salt (2.5% saline) containing bottles or were taken away. Suckling-induced PRL response was significantly decreased after 24 h and almost completely blocked 48 h later in dehydrated mothers. This effect could be prevented by haloperidol (a DA receptor antagonist) pretreatment (0.1 mg/kg BW sc), and it was only transient because rehydration of the mothers reestablished basal as well as suckling-induced PRL response. In addition, the effect of an acute osmotic stimulus on the plasma PRL levels (injecting 0.5 ml 10% saline solution iv) was also tested. There was a marked and immediate decrease in PRL concentration within 15 min of injection. Domperidone, another DA receptor blocker (20 micrograms/rat iv) completely abolished the depletion of plasma PRL in response to 10% saline injection. These results support our assumption that the dopaminergic regulation of PRL secretion during lactation involves the THDA system. Furthermore, these data underline the importance of an interaction between regulation of PRL secretion and water and sodium homeostasis.