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Experiments were performed to determine whether the suppression of prolactin (PRL) surges during restraint was accompanied by changes in the activity of tuberoinfundibular dopamine (TIDA) neurons in the median eminence. Animals were either ovariectomized and estrogen-treated (OVX-PEP) or cervically stimulated to induce pseudopregnancy (PSP). Restraint stress was administered by tying the hind legs together with plastic-coated bell wire. Animals were decapitated following 15 or 30 min of restraint stress or immediately after removal from the animal room (control) when PRL levels were basal (10.00 h), at the peak of the afternoon PRL surge in OVX-PEP animals (17.00 h) or the nocturnal PRL surge in PSP animals (05.00 h). Median eminence dopamine (DA) and dihydroxyphenylacetic acid (DOPAC) were significantly decreased in control rats at 17.00 h when compared to control rats at 10.00 h (103.1 +/- 3.7 vs. 85.8 +/- 3.3 and 11.4 vs. 7.1 +/- 0.4 pg/micrograms protein, respectively) and plasma PRL was markedly elevated. Restraint stress at 10.00 h resulted in a significant increase in serum PRL, but this increase was not accompanied by a change in DA or DOPAC when compared to control animals (103.1 +/- 3.7 vs. 107.9 +/- 4.8 and 11.4 +/- 0.4 vs. 10.4 +/- 0.6 pg/micrograms protein, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Prolactin activity was measured in serum, urine and milk using a specific human prolactin radioimmunoassay (RIA). Serum, urine and milk were parallel with the human prolactin standard in the RIA. There was no correlation between serum prolactin levels and urinary prolactin activity. Dialysis of urine samples resulted in complete loss of human prolactin activity while the addition of human prolactin to the urine resulted in the recovery of over 50% of the hormone after dialysis. Thus it was concluded that prolactin is not present in urine. In additional experiments it was observed that the RIA prolactin activity in urine was significantly correlated with the osmolality of the urine and that Na+ and K+ were contributory elements. On the other hand, prolactin was found in human milk and correlated well with the expected serum levels of this hormone. This latter finding is interesting because prolactin receptors have been shown to exist on the serosal side of the mammary epithelial cells. The presence of prolactin in milk suggests the possibility of other sites of action for this hormone in addition to the cell membrane.

The involvement of adrenergic, serotonergic and cholinergic mechanisms in the diurnal surge of plasma prolactin (Prl) secretion has been examined using ovariectomized, polyestradiol phosphate-treated (PEP) rats bearing aortic catheters. An afternoon surge in plasma Prl was observed to peak at 15.00 h and 17.00 h followed by declining levels at 19.00 and 21.00 h. This pattern was observed between 5 and 21 days after PEP administration. The alpha-adrenergic blocker, phenoxybenzamine (Phenox), completely prevented the Prl surge. The beta-blocker, propranolol (Propra), appeared to delay the onset and intensity of the diurnal Prl surge so that maximum levels were observed at 19.00 and 21.00 h. The serotonergic blocker, methysergide (MES), delayed the maximum diurnal Prl level until 21.00 h, while cyproheptadine (Cypro), another serotonergic blocker, significantly inhibited the surge. The muscarinic cholinergic agonist, arecoline (Arec), when administered at 12.00 h, delayed the surge, while the repeated administration of Arec completely blocked the surge. Atropine (Atro) (10 m/kg at 12.00 h and 5 mg/kg every 2 h thereafter) did not have any effect on the Prl surge, but when administered simultaneously with Arec, prevented the inhibitory effect of Arec on Prl release. The data suggested that the adrenergic and serotonergic systems have a positive input in the occurrence and magnitude of the surge and that the cholinergic system does not appear to have a physiologic role in tonically inhibiting Prl release, but may function under certain special conditions.

Female rats were neonatally androgenized (NA) by administering 1.25 mg of testosterone propionate at 3 days of age. At 21-23 days of age, groups of 12 animals each were blinded (BLD), olfactory bulbectomized (ANOS) and pinealectomized (PX) either alone or in combination. At 11 weeks of age all animals were ovariectomized, implanted with atrial catheters and given 0.5 mg polyestradiol phosphate. At 12 weeks of age, animals were attached to catheter extensions and blood samples obtained at 09.00, 11.00, 13.00, 15.00, 17.00, 19.00 and 21.00 h. The plasma prolactin (PRL) pattern of NA control animals consisted of elevated basal values at 11.00 and 13.00 h with an afternoon peak at 17.00 h. Anosmic and PX animals had a PRL pattern similar to that of the control. Animals BLD or BLD + ANOS had significantly lower plasma PRL values than sham-operated animals. Animals BLD + PX had PRL values comparable to PX alone. The diurnal PRL pattern observed for NA control animals was still evident in all experimental animals. Blinding + ANOS resulted in a significant decrease in ovarian and oviductal weights and attenuated the estrogen-induced increase in uterine weight. The evidence indicated that the elevated morning PRL levels observed in NA rats was not due to an altered function of the pineal gland and that BLD + ANOS blunted the action of exogenous estrogen on uterine weight.

It has been reported that the corticomedial amygdala (CMA) is involved in regulating various hypothalamic and neuroendocrine events. This study examined the role of the CMA in the regulation of the nocturnal surge of prolactin (PRL) induced by cervical stimulation (CS). Female Sprague-Dawley rats were ovariectomized, received CMA or sham lesions, and were placed on a reversed lighting schedule of 14 h light:10 h dark. 3 weeks later, all rats were cervically stimulated. 5 days after CS (CS + 5) rats were fitted with chronic, intraatrial catheters, and daily progesterone (P) injections (10 mg s.c.) were initiated. On CS + 8, CS + 12, and CS + 15, sequential blood samples were taken from unrestrained rats at 00.00, 02.00, 04.00, 06.00, 08.00, and 10.00 h (animal time). CMA lesions significantly reduced peak PRL levels on CS + 12 and CS + 15, but not on CS + 8. When ovariectomized CS rats received either 1 or 10 mg P/day and were sampled on CS + 12, CS + 15, and CS + 19, CMA lesions reduced the magnitude of the surge on CS + 12 and CS + 15, a time when P amplification of the surge was apparent. On CS + 19, when P amplification of the surge was absent, CMA lesions had no effect. CMA lesions greatly reduced peak PRL levels on CS + 12, but not on CS + 8, when rats were lesioned, catheterized, and injected daily with 1 or 10 mg P/day on CS + 3.(ABSTRACT TRUNCATED AT 250 WORDS)

Female Sprague-Dawley rats were ovariectomized, given estrogen, and blood samples were obtained via an atrial catheter in the afternoon during the prolactin (PRL) surge. Restraint stress applied at 16.00 h and continued for 3 h resulted in marked decrease in plasma prolactin (PRL) and an increase in plasma corticosterone (B). The neural mechanism(s) involved in the plasma PRL decrease to restraint stress in the afternoon were examined using neural agonists and antagonists. The administration of pimozide, a dopamine antagonist, increased plasma PRL and completely prevented the restraint-induced decrease in PRL. This result suggested that an increase in dopamine secretion mediated the stress-induced decrease of PRL in the afternoon. In unrestrained animals, the intravenous administration of atropine (a muscarinic cholinergic antagonist), arecoline (a muscarinic cholinergic agonist), propranolol (a beta-adrenergic antagonist) and morphine (a beta-endorphin agonist) at 16.00 h decreased plasma PRL from that of vehicle-injected animals. Bicuculline (a GABAergic antagonist) had no effect while phentolamine (an alpha-adrenergic antagonist) and phenoxybenzamine (an alpha-adrenergic antagonist) initially increased and then decreased plasma PRL. Naloxone (a beta-endorphin antagonist) initially decreased and then increased plasma PRL in unrestrained animals. In restrained animals, the intravenous administration of atropine and naloxone had no effect on the decrease in plasma PRL. Bicuculline and propranolol decreased plasma PRL below that observed for restrained animals alone, while phentolamine and morphine slightly retarded the course of the decrease. Arecoline did not alter the PRL decrease to restraint in the early sample periods but was followed by a rebound increase at later times.(ABSTRACT TRUNCATED AT 250 WORDS)

The influence of varying doses of perphenazine, thyrotropin-releasing hormone (TRH) and serotonin on prolactin release was examined in two species of monkeys: rhesus (Macaca mulatta) and crab-eating (Macaca fascicularis). The intravenous administration of 0.33 mg/kg body weight of perphenazine or 1.0 mug/kg body weight of TRH gave a greater release of prolactin than higher doses of perphenazine (1.0 mg/kg) or TRH) (3.4 mug/kg), respectively. Prolactin release induced by serotonin at doses of 1, 5 and 10 mug/kg was similar. Both atropine sulfate (Atr-SO4) and atropine methyl nitrate (Atr-MN) at a similar base level potentiated the prolactin releasing action of the high dose of perphenazine suggesting that high doses of perphenazine activate a cholinergic inhibitory component present in the pituitary. Atropine sulfate had no potentiating action on the TRH-induced prolactin release, while Atr-MN appeared to prolong the response of TRH without potentiating it. Neither form of atropine had any influence on serotonin-induced prolactin release. The data indicated that the lower prolactin response to high doses of perphenazine and TRH were brought about by different mechanisms, and that the mechanism for perphenazine appeared to be mediated through a pituitary cholinergic system.

Pseudopregnancy induced by cervical stimulation was inhibited by acute electrochemical stimulation of the corticomedial amygdala or dorsal hippocampus under sodium pentobarbital anesthesia (40 mg/kg) in adult, cyclic female Sprague-Dawley rats. The degree to which pseudopregnancy was blocked depended on temporal conditions of brain stimulation and sodium pentobarbital administration. Pentobarbital alone had a suppressing effect on the incidence of pseudopregnancy, especially when it preceded cervical stimulation. Limbic stimulation before cervical stimulation had a tendency to potentiate the suppression of pseudopregnancy by pentobarbital. After cervical stimulation, hippocampal stimulation tended to inhibit the development of pseudopregnancy, potentiating the pentobarbital suppression, while amygdala stimulation tended to override the pentobarbital blockage of pseudopregnancy. These findings suggest a negative influence of these two limbic structures and pentobarbital on the secretion of prolactin.

Electrochemical stimulation of the neocortex, VMH-arcuate hypothalamus, medial preoptic area, corticomedial amygdala, and dorsal hippocampus was performed under pentobarbital anesthesia to determine the brain regions involved in prolactin release as evidenced by pseudopregnancy. Stimulation occurred on the day of vaginal estrus, followed 4 days later by uterine traumatization. All animals were sacrificed 8 days after brain stimulation. Medial preoptic sitmulation resulted in an 83% incidence of pseudopregnancy while VMH-arcuate stimulation resulted in 43% incidence. Amygdaloid and hippocampal stimulation resulted in a lower incidence of pseudopregnancy (20 and 24%, respectively). Stimulation of the neocortex or sham stimulation of the five brain regions did not induce pseudopregnancy. These data indicate that the MPOA and VMH-arcuate hypothalamus are areas which may facilitate the release of prolactin necessary for the development of pseudopregnancy. The lower incidence of deciduomata formation resulting from electrochemical stimulation on the amygdala and hippocampus suggest that these areas have a minor effect on stimulating the induction of pseudopregnancy.