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L S Frawley

Publications and source records attributed to L S Frawley.

At least 55 records · Page 3Linked to original sources
PubMed1993

Lactotrope differentiation in rats is modulated by a milk-borne signal transferred to the neonatal circulation.

We have previously reported that normal differentiation of PRL-secreting cells in neonatal rats requires a maternal signal specific to the first few days of lactation. Subsequently, we found that milk proteins from this period had a greater capacity than those from later in lactation to stimulate lactotrope differentiation in vitro, suggesting that the maternal signal was a milk-borne peptide. We reasoned in the present study that if this were the case, the signal should be present in the serum of suckling pups, and its level should reflect that in mothers' milk. To test this hypothesis, we first compared serum from 3-day-old pups with that from newborn pups that had not yet suckled. Anterior pituitary cells from 1-day-old pups were cultured for 6 days in the presence of various serum samples (0.01-1.0% by volume). Lactotrope differentiation was assessed using a reverse hemolytic plaque assay for PRL. Serum from 3-day-old pups was more effective (P < 0.01; n = 4) than that from unsuckled newborns at stimulating lactotrope differentiation in vitro (to 3.5 +/- 0.5% and 1.5 +/- 0.5% of all anterior pituitary cells, respectively). Next, we tested whether this increase in serum bioactivity in 3-day-old pups required maternal influences restricted to the first few days of lactation. Newborn pups were placed with foster mothers that had been lactating for 0 or 7 days. When the pups were 3 days old, their serum was tested for lactotrope-differentiating activity. Serum from pups placed with day 0 foster mothers (control) increased the abundance of PRL cells to 2.4 +/- 0.3% of all cells (P < 0.01; n = 3), whereas serum from pups placed with day 7 foster mothers failed to stimulate lactotrope differentiation. In similar experiments, litters placed the day after birth with day 7 foster mothers were separated on day 3 postpartum for 3 h, after which littermates were allowed to suckle for 90 min on different foster mothers on day 3 or 9 of lactation. This brief suckling bout increased (P < 0.01; n = 3) the capacity of serum from pups on day 3 mothers to stimulate PRL cell differentiation (to 3.9 +/- 0.4%) above that of serum from littermates placed with day 9 foster mothers (to 1.8 +/- 0.2%). Finally, the differentiating activities in pup serum and mothers' milk eluted from gel filtration chromatography in identical fractions (4-8 kilodaltons).(ABSTRACT TRUNCATED AT 400 WORDS)

Aging↗
PubMed1993

Does alpha-melanocyte-stimulating hormone from the pars intermedia regulate suckling-induced prolactin release? Supportive evidence from morphological and functional studies.

Recent evidence suggests that substances derived from the hypophyseal intermediate lobe (IL) play a crucial role in the regulation of suckling-induced PRL secretion. The purpose of the present study was to explore this possibility further by determining whether the suckling stimulus acutely increases the secretory activity of the IL and whether alpha MSH, a major secretory product of the IL, plays a specific role in suckling-induced PRL release. Light microscopic morphometric analysis of serial pituitary sections obtained from lactating rats revealed that as little as 1 min of suckling caused a significant increase in the proportion of the IL that was in secretory configuration (11.8 +/- 0.7% vs. 6.7 +/- 0.5%; 1-min suckled vs. nonsuckled control; mean +/- SE). Moreover, the fraction of the IL in secretory configuration continued to increase after 5 and 10 min of nursing (to 16.0 +/- 0.8% at 5 min and 18.2 +/- 0.7% at 10 min). In contrast, serum PRL was not significantly elevated above the control level after 1 min of suckling (18.1 +/- 13.5 vs. 9.9 +/- 6.5 ng/ml, 1-min suckled vs. control). In fact, a significant rise in PRL levels (to 314.4 +/- 19.4 ng/ml) could be detected only after 10 min of nursing. Thus, secretion by the IL in response to suckling preceded the release of adenohypophyseal PRL, suggesting that a secretory product(s) from the pars intermedia is involved in the modulation of nursing-induced PRL release. Having established a sequential temporal relationship between these two phenomena, we next investigated whether alpha MSH was the IL factor involved in the regulation of suckling-induced PRL secretion. To this end, lactating rats were injected either with antiserum to alpha MSH or preimmune serum and then allowed to nurse their pups. Serial blood samples were taken from the mothers 15, 30, 60, and 90 min after the litters were returned, and serum PRL was measured by RIA. We found that the suckling-induced rise in serum PRL was severely attenuated in animals that received anti-alpha MSH serum. This suppression was most evident at 15 min (70.1 +/- 13.4 vs. 323.5 +/- 127.0 ng/ml, antibody treated vs. preimmune serum control) and persisted throughout the entire 90-min test period. When taken together, our results suggest that suckling-induced PRL secretion is mediated at least in part by alpha MSH released from the hypophyseal IL.

Animals↗
PubMed1993

Des-acetylated variants of alpha-melanocyte-stimulating hormone and beta-endorphin can antagonize the mammotrope-recruiting activity of their acetylated forms.

We have previously reported that hypophysial neurointermediate lobe peptides, di-acetylated alpha-melanocyte-stimulating hormone (di-ac-alpha-MSH) and N-acetylated beta-endorphin (N-ac-beta-END), can acutely increase the relative number of prolactin-secreting cells in anterior pituitary cell cultures from ovariectomized rats. Inasmuch as the des-acetylated forms of these peptides (des-ac-alpha-MSH and beta-END) were not effective in this regard, we concluded that acetylation was an absolute requirement for manifestation of the recruitment response. The aim of the present study was to determine whether these des-acetylated variants could antagonize the mammotrope-recruiting activity of their acetylated congeners. Treatment of anterior pituitary cell cultures with di-ac-alpha-MSH and N-ac-beta-END increased the relative amount of prolactin secretors above control values. Interestingly, des-acetylated variants of alpha-MSH and beta-END blocked the mammotrope-recruitment activity of their respective acetylated forms. In addition, beta-END antagonized the mammotrope-recruitment activity of di-ac-alpha-MSH while des-ac-alpha-MSH did not attenuate the stimulatory effect of N-ac-beta-END. Given that mammotropes maintained in vivo are exposed to all these peptides, it is possible that these acetylated and non-acetylated congeners may act in an opposing manner to regulate dynamic prolactin release.

Acetylation↗
PubMed1992

Acute recruitment of prolactin-secreting cells is regulated posttranscriptionally.

17 beta-estradiol (E2) stimulates the release of an activity from neurointermediate lobe (NIL) cells which increases the relative abundance of prolactin (PRL) secretors in cultures of anterior pituitary (AP) cells. In the present study, we sought to determine whether this NIL/E2 effect was due to recruitment of growth hormone (GH)-releasing cells into the PRL-secreting population and to define the mechanism regulating this induction of PRL secretors. AP cells from ovariectomized rats were cultured overnight, exposed to NIL/E2 treatment (or medium alone) for 3 h and then subjected to reverse hemolytic plaque assays for PRL and GH release. We found that exposure to NIL/E2 increased by 10% the proportion of AP cells that secreted PRL but did not influence the overall abundance of cells that released GH. A more critical analysis of these cultures revealed that all of the newly recruited PRL-secreting cells also released GH. This increment in the proportion of cells that released both PRL and GH concurrently was accompanied by an equivalent decrease in the fraction that secreted GH alone. Thus, it appeared that NIL/E2 treatment initiated PRL secretion by cells that previously released only GH. We then tested whether this induction of PRL secretors required the synthesis of proteins and/or RNA. We found that the protein synthesis inhibitor cycloheximide completely abolished the recruitment of PRL-releasing cells by NIL/E2 treatment, whereas the RNA synthesis inhibitor actinomycin D had no effect on this response. We conclude that NIL/E2 treatment induces PRL secretion by cells that formerly released only GH and that this induction is regulated posttranscriptionally.

Animals↗
PubMed1992

Alpha-melanocyte-stimulating hormone is a mammotrophic factor released by neurointermediate lobe cells after estrogen treatment.

When neurointermediate lobe (NIL) cells from ovariectomized rats are exposed to 17 beta-estradiol (E2) in vitro, they release a substance that rapidly induces the recruitment of additional PRL cells into the secretory pool. In the present study we tested the hypothesis that this mammotrophic factor is alpha MSH. Cocultures of anterior pituitary and NIL cells were incubated for 18 h, exposed to various treatments for 3 h, and then subjected to a reverse hemolytic plaque assay to quantify the percentage of all pituitary cells that released PRL. Combined exposure to E2 and NIL cells caused a significant increase in the fraction of anterior pituitary cells that released PRL, and the presence of TRH during the reverse hemolytic plaque assay did not affect the magnitude of the response. Treatment with dopamine (which inhibits alpha MSH release) reversed the recruitment of PRL secretors induced by E2 stimulation of NIL cells. Likewise, immunoneutralization with an antiserum directed against alpha MSH abolished the response. Furthermore, alpha MSH alone could substitute for E2 and NIL cells in evoking the recruitment response, whereas none of several other POMC-derived peptides had any consistent effect. Taken together, these results demonstrate that alpha MSH is a mammotrophic factor released by NIL cells in response to E2.

Animals↗
PubMed1992

Steroids can modulate transdifferentiation of prolactin and growth hormone cells in bovine pituitary cultures.

Fluctuations in the proportions of pituitary acidophils (cells that release GH and PRL, either separately or concurrently) have been correlated with dynamic changes in the steroid hormone milieu. Since modulation of these acidophilic subtypes can occur without appreciable alterations in the total number of acidophils, it has been proposed that GH- and PRL-secreting cells can actually transdifferentiate (gain or lose the ability to release GH or PRL). To test this hypothesis, we examined the effects of steroids on the proportions of cells that released GH, PRL, or both hormones (i.e. mammosomatotropes) in bovine pituitary cell cultures. Specifically, anterior pituitary cells from castrated males were cultured for 6 days in the absence (controls) or presence of 17 beta-estradiol, cortisol, or progesterone. Reverse hemolytic plaque assays revealed that 6.64 +/- 1.2% of all pituitary cells released GH, while 68.8 +/- 5.3% were PRL secretors in control cultures. Cortisol and progesterone induced an increment in the proportions of GH-secreting cells (10 nM cortisol, +11.7 +/- 2.4%; 1000 nM cortisol, +10.5 +/- 4.7%; 1000 nM progesterone, +2.87 +/- 1.5%) above control values while decreasing the relative abundance of cells that released PRL (10 nM cortisol, -7.6 +/- 1.7%; 1000 nM cortisol, -6.6 +/- 1.2%; 1000 nM progesterone, -5.5 +/- 1.3%) below control values. However, 17 beta-estradiol was ineffective in this regard at doses of 0.1-1000 nM. A more critical examination of the steroid-induced changes revealed that they were attributable to increases in the proportions of cells that released GH alone and both hormones simultaneously along with a concomitant decrease in the fraction that secreted only PRL. Two lines of evidence discount the possibility that these effects were due to selective cell proliferation. First, the mitotic rate of cultures (assessed by immunofluorescent detection of bromodeoxyuridine incorporation) was only about 1% of all cells in both control and steroid-treated cultures. Second, blocking cell proliferation by the addition of cytosine arabinoside (100 microM) did not inhibit the cortisol-induced augmentation of GH-releasing cells. Taken together, these results substantiate the hypothesis that acidophilic subpopulations are capable of transdifferentiation given an appropriate hormonal signal.

Animals↗
PubMed1992

N-acetylation is required for the lactotrope recruitment activity of alpha-melanocyte-stimulating hormone and beta-endorphin.

Pituitary neurointermediate lobe (NIL) cells obtained from ovariectomized rats and exposed to 17 beta-estradiol in vitro have been shown to release an activity that induces acute recruitment of additional PRL-secreting cells. We have recently reported that alpha MSH, a major secretory product of the NIL, can substitute for this lactotrope-recruiting factor released by NIL cells in response to 17 beta-estradiol. beta-Endorphin (beta END) was not effective in this regard. Inasmuch as the degree of acetylation is critical to the activities of both of these molecules in other systems, we decided to assess its importance to lactotrope-recruiting activity in the present study. Anterior pituitary cells from ovariectomized rats were cultured overnight, exposed to various treatments for 3 h, and then subjected to a reverse hemolytic plaque assay for PRL. Exposure to mono- and diacetylated alpha MSH (N-ac-alpha MSH and di-ac-alpha MSH, respectively) or N-acetylated beta END (N-ac-beta END) caused a significant increase in the fraction of anterior pituitary cells that released PRL. In contrast, the Des-acetylated variants of both molecules had no lactotrope-recruiting activity. In a dose-response study, maximally effective doses of di-ac-alpha MSH and N-ac-beta END were equally effective with respect to their function as lactotrope-recruiting factors. Furthermore, the two peptides acted cooperatively when simultaneously applied in submaximal concentrations. Taken together, these results demonstrate that 1) N-acetylation is an essential requirement for the lactotrope-recruiting activity of alpha MSH and beta END in vitro; and 2) di-ac-alpha MSH and N-ac-beta END can act in a cooperative fashion to recruit additional cells into the PRL-secreting population.

Acetylation↗
PubMed1992

Neurointermediate lobe peptides recruit prolactin-secreting cells exclusively within the central region of the adenohypophysis.

There is strong evidence that the hypophyseal neurointermediate lobe (NIL) mediates 17 beta-estradiol (E2)-induced PRL secretion in rats. Our laboratory has previously demonstrated that E2 stimulates NIL cells to release an activity that acutely increases the relative abundance of PRL-releasing cells in anterior pituitary (AP) cell cultures. We later found that secretory products of the NIL melanotropes, specifically the acetylated forms of alpha MSH and beta-endorphin (beta END), can account for this activity. Given that blood from the NIL initially perfuses the region of the AP proximal to the NIL, we tested the hypothesis that this specific area was preferentially responsive to the lactotrope recruitment activities. AP glands from ovariectomized rats were dissected into an inner zone, proximal to the NIL, and the remaining outer zone of the gland, then dispersed with trypsin. The resulting cells were cultured for 16 h, either alone or in coculture with NIL cells, and subsequently treated with medium alone (control) or with alpha MSH, beta END, or E2 (all at 1 x 10(-7) M) for 3 h and then subjected to reverse hemolytic plaque assays for PRL release. Under control conditions, the proportion of PRL-secreting cells was significantly greater in cultures from the outer zone of the AP than in those from the corresponding inner zone of the gland. Treatment of AP cells from the inner zone with alpha MSH, beta END, or the E2-induced NIL activity significantly increased the percentage of PRL secretors by about 8% of all AP cells. In contrast, the fraction of PRL-secreting cells in cultures from the outer zone was not affected by these treatments. We conclude that the recruitment of PRL-secreting cells in response to products of the NIL occurs only in that region of the AP proximal to the NIL.

Animals↗
PubMed1992

The ontogenic and functional relationships between growth hormone- and prolactin-releasing cells during the development of the bovine pituitary.

The ontogeny of GH- and prolactin-releasing cells in the developing bovine pituitary was evaluated by reverse haemolytic plaque assays which allows for the detection of hormone release from individual pituitary cells in culture. With this approach, we observed that GH-releasing cells ontogenically preceded prolactin-releasing cells. In fact, GH secretors were observed as early as 59 days of gestational age while cells that released prolactin were not identified until 98 days. The amounts of both GH- and prolactin-releasing cells increased with time to reach more than 50% and 20% of all pituitary cells near term (term approximately 280 days) respectively. Interestingly, the first cells shown to release prolactin also released GH (i.e. were mammosomatotropes). This temporal and functional relationship between GH and prolactin secretors provides suggestive evidence that GH-secreting cells act as the progenitor cells for prolactin secretors via a functional intermediate, the mammosomatotrope.

Animals↗
PubMed1992

Suckling reverses mammotrope responsiveness to TRH.

It is well established that suckling can alter the responsiveness of mammotropes to the prolactin (PRL) releasing actions of thyrotropin-releasing hormone (TRH). The purpose of the present study was to more critically characterize this phenomenon and to determine whether this effect was manifested at the point of TRH receptor binding and effector coupling. Cultured anterior pituitary (AP) cells from suckled and nonsuckled rats were subjected to reverse hemolytic plaque assays for PRL in the absence or presence of TRH. Treatment with TRH (100 nM for 2 h) significantly stimulated PRL secretion by pituitary cells from transiently suckled females (to 147.0 +/- 0.7% of control value; P < 0.05). Surprisingly, this same dose of the secretagogue caused a 30% inhibition (P < 0.05) of PRL release by AP cells obtained from nonsuckled lactators. In order to gain some insight into the possible mechanisms that govern these drastic changes in mammotrope responsiveness to TRH, we evaluated the ability of this secretagogue to activate the phosphoinositidase pathway. To this end, we chose to measure the intracellular accumulation of inositol monophosphate (IP1), a degradative metabolite of the inositol 1,4,5-triphosphate (Ins 1,4,5-P3) second messenger molecule, in the presence of LiCl (10 mM) which prevents further metabolism of IP1. We found that a 2 h exposure to 100 nM TRH resulted in a 3-fold increase in IP1 accumulation by AP cultures derived from both suckled and nonsuckled dams. Our results indicate that TRH effectively activates its receptor and couples to the phosphoinositidase pathway in AP cells from both nonsuckled and suckled females. Thus, we conclude that the suckling-induced increase in mammotrope responsiveness to TRH is regulated subsequent to TRH receptor activation.

Animals↗
PubMed1991

The suckling stimulus increases the responsiveness of mammotropes located exclusively within the central region of the adenohypophysis.

Studies from several groups, including our own, have shown that the suckling stimulus increases the responsiveness of pituitary cells to PRL-releasing stimuli. These findings, when viewed in light of differences in PRL cell responsiveness from one pituitary region to another, raised the possibility that suckling may influence responsiveness of cells in only a specific portion of the gland rather than in the entire pituitary. To address this issue, we evaluated cell responsiveness by performing plaque assays [with and without TRH, Angiotensin II (AII), and dopamine] on cells from two different regions of pituitaries from suckled and nonsuckled rats. These pituitary regions consisted of the inner zone, which is a central area proximate to the neurointermediate lobe, and an outer zone, which encompasses the remaining peripheral area of the anterior lobe. We found that inner zone cells from nonsuckled animals were highly responsive to dopamine and relatively unresponsive to TRH and AII. However, after suckling, a complete shift occurred with inner zone cells becoming sensitive to TRH and AII and resistant to dopamine. In contrast to these inner zone alterations, outer zone cells did not change after suckling, but remained responsive to TRH and AII and unresponsive to dopamine. Our results demonstrate clearly that suckling-induced alterations in PRL cell responsiveness to certain modulatory agents can be attributed to a discrete subpopulation of cells located in a specific region of the pituitary.

Angiotensin II↗
PubMed1991

Normal differentiation of prolactin cells in neonatal rats requires a maternal signal specific to early lactation.

This laboratory has previously demonstrated that PRL-secreting cells are virtually nonexistent on day 3 but appear in appreciable numbers on day 4 of neonatal life. The purpose of the present study was to determine whether this explosive appearance of PRL cells is due to maternal influences specific to the first 4 days of lactation. Litters of 1-day-old rat pups were placed with foster mothers that had been lactating for either 1 or 4 days. Four days later (at 5 days of age), the anterior pituitaries from these pups were removed, dispersed into individual cells with trypsin, and subjected to reverse hemolytic plaque assays for PRL and GH release. We found that the proportion of PRL-releasing cells in pituitaries from pups placed with day 1 mothers (4.2 +/- 0.6%; mean +/- SE; n = 4 experiments) was similar to that in 5-day-old pups that had not been fostered (3.4 +/- 0.6%; n = 3 experiments). In contrast, placing 1-day-old pups with day 4 mothers significantly reduced (P less than 0.01) the fraction that released PRL to 0.6 +/- 0.2% of all pituitary cells (n = 4 experiments). This effect appeared to be specific to PRL cells, since the percentage of all pituitary cells that secreted GH was not different between litters fostered onto day 1 or day 4 dams (40.0 +/- 3.8% and 41.1 +/- 3.9%, respectively; n = 3 experiments). Furthermore, the suppression of PRL cell expression did not result from a gross nutritional deficit, since the rates of body wt gain during the foster period were not different between the two groups (12.4 +/- 0.5 and 12.9 +/- 0.8 g/litter.day, respectively; n = 4 experiments). In a second design, newborn pups were placed with females that had been lactating for 0, 2, 4, or 7 days and analyzed for PRL- and GH-releasing cells at 5 days of age. In two trials of this experiment, the fractions of pituitary cells that secreted PRL were 5.2, 6.3, 5.9, and 1.2%, respectively for trial 1 and 3.3, 4.1, 0.7, and 0.6%, respectively for trial 2. As in the first experiment, the proportion of GH-releasing cells and the rate of growth were not different among the four groups. Taken together, these results indicate that normal differentiation of PRL cells in neonatal rats is triggered by a maternal signal present during the first few days of lactation, and that the magnitude of this signal declines with the progression of lactation.

Aging↗
PubMed1991

Mammosomatotropes are abundant in bovine pituitaries: influence of gonadal status.

Mammosomatotropes--cells that secrete both GH and PRL--are a common pituitary cell type in a variety of mammalian species. Recently, immunogold electron microscopy was used to demonstrate that all acidophils (a generic term used here to denote cells which secrete GH and/or PRL) in cattle stain for both GH and PRL. This high degree of overlap, which is unique among the mammalian species examined in this regard, raises the question: do all acidophils actively release both hormones concurrently? In the present study, we addressed this question by employing reverse hemolytic plaque assays to measure GH and PRL release from individual bovine pituitary cells in culture in the presence of stimulatory secretagogues. Inconsistent with the previous reports on hormone storage, all bovine acidophils in gonad-intact and castrated males did not actively release both GH and PRL. In gonad-intact males approximately 9% of all pituitary cells released both hormones, whereas 21% released only GH and 45% PRL alone. In castrated males, mammosomatotropes comprised only 22% of the pituitary cell population, whereas GH-only cells accounted for 8% and PRL secretors 46%. This divergence in the relative proportions of GH-only cells and mammosomatotropes suggests that the hormonal milieu plays an important role in maintenance of the various acidophilic cell types. In addition, the reciprocal relationship between cells that released GH-only and dual hormone secretors in the two models studied supports the possibility that these cell types are functionally interconvertible.

Animals↗
PubMed1991

Rapid augmentation of prolactin cell number and secretory capacity by an estrogen-induced factor released from the neurointermediate lobe.

17 beta-Estradiol (E2) has been shown to exert an acute stimulatory effect on PRL secretion via an indirect action involving the neurointermediate lobe (NIL). In the present study we used a reverse hemolytic plaque assay to determine whether this effect was manifested as an augmentation of the number of PRL secretors and/or an increase in the amount of hormone released per PRL cell. Cultures of anterior pituitary (AP) and NIL cells from ovariectomized rats were cultured overnight, exposed to the treatment (E2 or vehicle) for 3 h, and then subjected to a reverse hemolytic plaque assay that was carried out in the presence or absence of TRH. Concurrent exposure of AP cells to E2 and NIL cells evoked an 11-12% increase in the overall proportion of PRL-secreting cells. This was true when the AP and NIL cells were incubated as a mixed culture and when the two cell types were maintained in the same petri dish but on separate plastic supports, and TRH did not significantly influence this response. The effect of E2 on the number of PRL secretors was negated when NIL cells were not present throughout the experiment or when they were removed from the cultures just before commencement of E2 treatment. Simultaneous treatment with E2 and NIL cells also significantly augmented the sizes of PRL plaques produced under basal conditions by AP cells. Taken together, these results demonstrate that E2 stimulates NIL cells to release an activity that enhances PRL secretion in two ways: 1) by recruiting additional PRL cells into the secretory pool, and 2) by augmenting the secretory capacity of individual PRL cells.

Animals↗
PubMed1991

Suckling unmasks the stimulatory effect of dopamine on prolactin release: possible role for alpha-melanocyte-stimulating hormone as a mammotrope responsiveness factor.

Mounting evidence indicates that dopamine (DA) can stimulate as well as inhibit PRL release when given in appropriately low doses. In the present study, we investigated whether the suckling stimulus could influence this response. Pituitary cultures from suckled or nonsuckled rats were exposed to DA (10(-16) - 10(-6) M) during a reverse hemolytic plaque assay for PRL. Pituitary cells from nonsuckled rats exhibited only the inhibitory response to DA; exposure to high-dose DA (10(-6) M) reduced plaque area to 42.3 +/- 7.2% (mean +/- SEM) of control. A low dose of DA (10(-12) M) had no effect on PRL secretion (79.3 +/- 13.3% of control). In striking contrast, a brief suckling stimulus (10 min) rendered the mammotropes responsive to stimulation by low-dose DA (to 152.7 +/- 12.5% of control). Thus, suckling appears to be a requirement for expression of the stimulatory effect of DA in lactators. In a subsequent series of experiments we explored the possibility that a hypophysial factor, released during nursing, might mimic the effects of suckling on mammotrope responsiveness. Accordingly, we tested the effects of alpha-melanocyte-stimulating hormone (10(-7) M) and low-dose DA, alone or in combination, on pituitary cells from nonsuckled rats. Although neither agent alone had a dramatic effect on PRL secretion, concurrent administration of both of these significantly stimulated PRL release to 130.0 +/- 4.2% of control. Taken together, these results demonstrate that suckling renders mammotropes responsive to the stimulatory effects of DA. Moreover, our data indicate that alpha-melanocyte-stimulating hormone could function as a responsiveness factor in this phenomenon.

Animals↗
PubMed1991

Evidence for bidirectional interconversion of mammotropes and somatotropes: rapid reversion of acidophilic cell types to pregestational proportions after weaning.

The progression from nonpregnancy through late lactation is associated with an increase in the proportion of anterior pituitary cells that secrete PRL and a comparable decrease in the percentage of cells that release GH. These fluctuations result from variations in both the number of cells that release GH or PRL alone and mammosomatotropes, cells that release both hormones concurrently. However, it has not been determined whether this reciprocal shift in PRL and GH secretors during the onset of lactation is readily reversible. In the present study, anterior pituitaries from adult virgin, late lactating, or postweaning female rats (4, 6, or 8 days) were dispersed with trypsin and subsequently assayed for PRL and GH release using reverse hemolytic plaque assays. We found that separating lactating females from their pups for only 4 days induced a reciprocal shift in the proportions of GH and PRL cells back to levels found in virgin females. Simultaneous plaque assays were then performed to determine whether this post-weaning shift in the percentages of GH and PRL secretors was due to changes in the abundance of cells that secrete each hormone alone or in the proportion of mammosomatotropes. The overall changes in GH and PRL cell proportions consisted of variations only in the fraction of cells that secreted either GH or PRL alone; no differences were observed in the percentage of mammosomatotropes or in the overall abundance of acidophils. Our results demonstrate that the reciprocal shifts in the proportions of PRL- and GH-secreting cells associated with lactation are rapidly reversible. Moreover, these results are consistent with our hypothesis that PRL and GH secretors are functionally interconvertible and further suggest that this process is bidirectional.

Animals↗