Autoregulation of Prolactin Secretion in the Rat

Abstract

There is abundant evidence suggesting that prolactin (PRL) inhibits PRL secretion by short-loop feedback. To further characterise this modulatory effect of prolactin, this study reports on the effects of intrahypothalamic grafts of anterior pituitary tissue on prolactin secretion by the in situ pituitary. Blood samples were collected serially via indwelling aortic catheters or acutely by rapid decapitation, during the estrous cycle, pregnancy, and lactation. Serum samples were assayed using NIAMD radioimmunoassay materials. Intrahypothalamic grafts did not alter the tonically low levels of prolactin seen in the unstimulated state when grafted rats were compared with normal controls. Also, intra-hypothalamic grafts did not alter the normal prolactin increases which follow stimuli such as nursing or ether stress. In contrast, grafts completely abolished surge-like PRL increases which follow stimuli such as mating and estrogen. These findings suggest the existence of a rostrally located hypothalamic 'autoregulatory center' which prevents the expression of PRL surges. It was suggested that prolactin release from the graft into surrounding areas of the recipient's hypothalamus triggers the 'autoregulatory center' which in turn prevents the normal prolactin secretory response to mating and estrogen. A second series of experiments characterised the pattern of prolactin secretion in concurrently pregnant and lactating rats. It was shown that nocturnal surges of PRL secretion associated with pregnancy were potently inhibited by nursing. It was suggested that mating-stimulated PRL surges were suppressed by short-loop feedback because levels of PRL in systemic blood are sustained at high levels by nursing stimuli. Thus, this study apparently demonstrates for the first time the autoregulation of PRL secretion in a physiologic situation. Based on these findings and others, it was hypothesised that PRL in both systemic and retrograde blood is transported to separate 'autoregulatory centers' which in turn modulate different modes of PRL secretion.