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The biological activity and immunoreactivity of serum prolactin (PRL) has been shown to fluctuate throughout the estrous cycle of the rat. Since the 24-kDa nonphosphorylated and phosphorylated isoforms from several species have also been shown to differ in their biological and immunoreactivities, we have investigated the possibility that the 24-kDa monomer isoform profile varied throughout the estrous cycle of the rat. The PRL isoform profile was assessed in homogenates of pituitaries and in short-term incubation media. Comparisons between homogenates, which always contained isoforms 1, 2, 3, and 3' (numbered according to increasing acidity), and media showed nonproportional release of the isoforms at all stages. Of great interest were the release of isoform 1 (a nonphosphorylated form) only at estrus and the lack of release of isoform 3' (a phosphorylated form) only in the afternoon of proestrus. This lack of release of 3' was accompanied by a marked increase in the release of isoform 2 (the unmodified polypeptide). These results suggest a unique function for isoform 1 during estrus and a role for increased isoform 2 and absent isoform 3' during the proestrus surge of PRL. Moreover, they suggest that fluctuations in the biological activity and immunoreactivity of serum PRL during the estrous cycle could be due, at least in part, to fluctuations in the isoform profile.

We studied the effect of histamine on serum prolactin and thyrotropin (TSH) levels in male rats with anterolateral hypothalamic deafferentation of hypothalamic connections or anterolateral cut (ALC). The success of ALC was confirmed by immunohistochemistry of somatostatin (SRIF) in the medial basal hypothalamus. ALC did not affect basal prolactin or TSH levels. Thyrotropin-releasing hormone (TRH, 200 ng/rat, i.p.) did not affect prolactin secretion either in sham-operated or ALC rats. In sham-operated rats intracerebroventricularly administered histamine increased significantly prolactin levels. Hypothalamic deafferentation abolished the effect of histamine on prolactin levels. TRH increased significantly serum TSH levels both in sham-operated controls and ALC rats. In the latter, however, the TSH-secretory response to TRH was significantly (p less than 0.05) larger compared to the controls. Intracerebroventricularly infused histamine (2 micrograms/rat) did not change the TRH-induced TSH secretion in either group of rats. These results show that (1) the effect of histamine on prolactin secretion is mediated through nerve tracts which are destroyed by ALC, and (2) cutting of afferent TRH (through sensitization) and SRIF fibers (through lacking inhibition) entering medial basal hypothalamus may both contribute to the enhanced TSH response to exogenous TRH.

Serum prolactin was measured in lightly etherized rats between 4 and 5 a.m. and between 11 a.m. and 12 noon at various times after operation in intact rats and rats that had been operated on. Serum prolactin was elevated in the late nocturnal samples from intact rats and this elevation was prevented by pinealectomy. With time following the operation, daytime serum prolactin was also lowered in pinealectomized animals. In animals rendered anosmic by olfactory bulb removal, serum prolactin was also lowered. Superimposed pinealectomy only lowered late nocturnal serum prolactin in anosmic rats. Blinding the rats by ocular enucleation lowered nocturnal serum prolactin initially and dampened the daily rhythm in prolactin, but superimposed pinealectomy had no effect on the blinded animals. The combined sensory deprivation produced by both blinding and olfactory bulb removal resulted in low prolactin titers regardless of whether blood samples were taken during the day or late at night and, as in the case of blinded animals, there was no effect of pinealectomy. Superior cervical ganglionectomy also lowered serum prolactin. Serum prolactin declined following castration in intact animals and this decline was accentuated by pinealectomy. Either blinding or anosmia also lowered serum prolactin in the castrated animals but, as in intact animals, pinealectomy had little effect on the sensory-deprived rats. A further lowering of prolactin occurred in castrated animals which were both blinded and anosmic; in these animals, pinealectomy again had no additional effect. Measurement of the pituitary prolactin content in the castrated animals at sacrifice revealed a significant lowering of values in blinded animals, with restoration of the values to control levels by pinealectomy. Anosmia also lowered the pituitary prolactin content but this was not reversed by pinealectomy. The lowest pituitary prolactin was found in blinded, anosmic animals and these changes were not reversed by pinealectomy. The weight of the pineal gland increased significantly in anosmic, blinded, or blinded and anosmic rats. It is concluded that pineal secretions in the male rat elevate serum prolactin, particularly late at night, and that loss of input from olfactory and to a lesser extent from visual pathways results in a decrease in the titer of the hormone. This decrease is especially apparent in blinded, anosmic rats.

Serum prolactin levels following ether anesthesia and laparotomy were measured in intact, cyclic rats which were injected daily, beginning on the first day of diestrus, with either oil or with 2 (P2) or 10 mg (P10) of progesterone. A single P2 or P10 injection affected neither the basal (decapitation) nor the ether-laparotomy serum prolactin level. Six days of treatment, however, reduced the ether-laparotomy-induced in-crease in the prolactin level, but had no effect on the basal level. Ovariectomized rats were also injected daily for 6 days, beginning on the 14th post-castration day, with either oil, P10,0.01 (E 0.01) or 0.25 µg (E 0.25) of free estradiol, or a combination of either E 0.01 + P10 or E 0.25 + P10. No significant differences in the serum prolactin levels were found between the rats killed by decapitation and those subjected to ether-laparotomy in any of these groups. Treatment with P10, however, significantly lowered the serum prolactin level although treatment with E 0.25 raised it. P10 treatment also reduced the estrogen (E O.25)-stimulated elevation in the prolactin level.

The effect of breast feeding on serum FSH and LH concentrations was studied in 13 puerperal women. Despite the collateral increase in serum prolactin levels, nursing was not followed by significant changes in serum FSH or LH levels during a 30-min observation period. Our data indicate that nursing has no significant effect on pituitary FSH and LH release.

Rat strains selectively bred for behavioral differences in susceptibility to mild stress exhibited differences in serum prolactin (Prl) and hypothalamic dopamine (DA). Male rats from the Maudsley Reactive (MR) strain had higher levels of serum Prl and hypothalamic DA than rats from the Maudsley Non-Reactive (MNRA) strain. MR rats also showed a greater percentage increase in serum Prl 1 h after blockade of catecholamine synthesis by administration of alpha-methylparatyrosine (alphaMpT). The correlation of basal serum Prl levels with individual susceptibility to stress constitutes further evidence that Prl may play a functional role in the organism's response to stress. Strain differences in hypothalamic DA function may play a role in the etiology of strain differences in serum Prl.

The binding of [3H]-spiperone to partially purified rat anterior pituitary plasma membranes was quantified throughout the estrous cycle in relation with the serum prolactin (PRL) levels. Re

The intraperitoneal (i.p.) administration of sodium pentobarbital (30 mg/kg) to long-term ovariectomized adult rats results in a prolonged depression of serum LH levels and in a biphasic decrease of serum prolactin (Prl) titers, but does not modify serum levels of FSH. Consequently, caution should be used when interpretating neuroendocrine results obtained in animals submitted to pentobarbital anesthesia.

At 1 h after a single subcutaneous injection of haloperidol into early proestrous rats, there was an 11-fold elevation in serum prolactin. Pituitary prolactin concentration 4 h after administration of

Studies were carried out to investigate the negative feedback effect of progesterone on the secretion of prolactin (Prl). Ovariectomized adult rats were treated with either 50 μ g of

Complete isolation of ablation of the medial basal hypothalamus (MBH) was performed in adult male rats, and non-stress prolactin levels were measured by radioimmunoassay in blood collected by decapitation at 24h, 2 weeks and 6 weeks following surgery. 24 h after surgery, medial hypothalamic ablation (MHA) markedly elevated prolactin levels compared to those of intact control rats; prolactin levels subsequently declined to normal resting values 2 to 6 weeks following surgery. Circulating prolactin levels following hypothalamic isolation were not different from those of controls at either acute or chronic sampling intervals. These data suggest that chronic isolation or destruction of the MBH does not alter basal prolactin secretion in male rats, provided that circadian and stress-induced variations in control animals are properly considered.

A number of centrally active benzodiazepines lowered baseline serum prolactin concentrations after oral administration to male rats. The increase of circulating prolactin levels elicited by oral administration of various neuroleptic agents was also reduced by prior or simultaneous oral administration of several benzodiazepines in a dose-dependent manner. Since both effects were prevented by simultaneous administration of the benzodiazepine antagonist Ro 15-1788 they are probably mediated by central benzodiazepine receptors which interfere with aminergic mechanisms governing serum prolactin.

Serum prolactin (Prl) was measured following decapitation at various stages of the estrous cycle in control animals and following cervicovaginal stimulation with a glass rod. Serum Prl was low at 10.00 h at all stages of the estrous cycle but was elevated on the afternoon of proestrus with peak values at 16.00 h and on the afternoon of estrus with peak values at 13.00 h. Cervicovaginal stimulation resulted in 100% incidence of pseudopregnancy when performed on estrus and diestrus I and in a still high incidence when performed on proestrus. However, on diestrous day II, it caused only delayed pseudopregnancy in less than half the rats. Serum Prl was significantly elevated in the afternoon following stimulation on diestrous day I and on estrus, but the already elevated values on proestrus were not further augmented and there was no significant elevation on diestrous day II. Thus, there was a cyclic variation in the response of Prl to cervicovaginal stimulation which correlated with the incidence of immediate pseudopregnancy. Gonadal steroids at this stage of the cycle probably modulate the reflex release or Prl either by an action at the hypothalamic or pituitary level or at both sites. On the basis of evidence provided by others, the immediate release of Prl does not appear to be required for the induction of pseudopregnancy.

Vaginal stimulation (VS) in virgin female rats on the first day of estrous induces a significant increase in serum prolactin levels 15 min, 6,9,10 and 12 h after stimulation. Normal level values were observed 2 h after VS but a significant decrease appeared 8 h after VS. In nonstimulated rats a significant variation was observed, with a peak at 10.00 and 18.00 h and minimal values at 12.00 and 16.00. Adenohypophysial prolactin concentration showed a significant decrease both 15 min and 6 h after VS. A significant increase occurred 4 h after VS. At 8, 9, 10 and 12 h after cervical stimulation, the levels of prolactin were similar to levels in the control rats. The curve obtained in nonstimulated rats showed a significant decrease between 10.00 and 12.00 h; the rest of the curve showed no significant variation. The levels of prolactin in the hypophysis and serum during the first 12 h after VS clearly show a phasic release of the hormone and a correlation between synthesis and release, suggesting the existence of some kind of neural hormonal factor of regulation.