Electrical potentials and cell-to-cell dye movement in mouse mammary gland during lactation

Berga, Sally E.

doi:10.1152/ajpcell.1984.247.1.c20

Cited by 43 publications

(25 citation statements)

References 24 publications

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“…The average resting membrane potential of mammary epithelial cells cultured in the absence of hormones was -33 ± 12 mV (mean ± SD, n = 70). Similar membrane potentials have been reported for mammary epithelial cells in the lactating rat (16,17). There was no difference in the membrane potential of cells during 7 days of culture.…”

Section: Results Electrical Properties Of the Membrane Of Mouse Mammarysupporting

confidence: 87%

Induction of distinct types of spontaneous electrical activities in mammary epithelial cells by epidermal growth factor and insulin.

Enomoto¹,

Cossu²,

Edwards³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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Electrophysiological measurements of the membrane potentials of mouse mammary epithelial cells in primary culture revealed the presence of spontaneous-oscillating-hyperpolarizing potentials in cells incubated with epidermal growth factor. The hyperpolarizing potentials were 5-20 mV in amplitude and about 10 sec in duration. The peak height of the response was reduced by hyperpolarization, and the input membrane resistance decreased during the response. The response was probably due to activation of K+ channels. The latency period for the epidermal growth factor induction of the hyperpolarizing potential was approximately 3 hr. In contrast, insulin induced spontaneous-depolarizing potentials that were about 5 mV in amplitude and 1 sec in duration. The depolarizing potentials were attributed to activity of ion channels, since the peak height was dependent on the membrane potential and the depolarizing potential was accompanied by a decrease of input membrane resistance. The time lag for the induction of the depolarizing potential was 6-12 hr. Other hormones involved in mammary cell differentiation, such as cortisol and prolactin, neither induced the depolarizing potentials nor changed the induction of depolarizing potential by insulin. In addition, other growth factors, such as nerve growth factor and fibroblast growth factor, elicited no electrical activity.The growth and differentiation of the mammary epithelium are regulated by a variety of peptide and steroid hormones (reviewed in refs. 1-3). In primary culture the synergistic actions of insulin, cortisol, and prolactin enhance the synthesis of milk components of mammary epithelial cells (4-7). In contrast, epidermal growth factor (EGF) stimulates proliferation of the mammary epithelium, both in vitro (6-8) and in vivo (9). Thus, mammary epithelial cells are a useful system in which to study the basic mechanisms of hormone action on cell growth and differentiation. (14) and fibroblasts (15). Alteration of ion-transport properties of the cell membrane has been suggested to be a key step in the regulation of cell growth. Thus, it is possible that some polypeptide hormones affect the permeability of ion channels in the cell membrane and that the movements of ions through such channels have important roles in the processes of cell proliferation and differentiation.To determine whether the movements of ions across the membrane of mammary epithelial cells are coupled with hormone actions, we examined the effects of these hormones and growth factors on the membrane potential and electrical activity of these cells by electrophysiological techniques. In this paper, we report that EGF and insulin induce two different membrane potential changes by modulating the activity of ion channels in cultured mammary epithelial cells. MATERIALS AND METHODSMaterials were obtained from the following sources: medium 199 (Hanks' salts) from GIBCO; bovine serum albumin from Miles-Yeda (Rehovot, Israel); bovine prolactin from the Hormone Distribution Program, National Institute ...

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Section: Results Electrical Properties Of the Membrane Of Mouse Mammarysupporting

confidence: 87%

Induction of distinct types of spontaneous electrical activities in mammary epithelial cells by epidermal growth factor and insulin.

Enomoto¹,

Cossu²,

Edwards³

et al. 1986

Proc. Natl. Acad. Sci. U.S.A.

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“…In contrast, during lactation no tracer could be observed in the bloodstream, and all injected tracer remained within the mammary gland until removed by milking. Similar results were obtained by Berga in the lactating mouse (Berga 1984). Linzell & Peaker (1971, 1974 also showed that [ 14 C]sucrose moved from the bloodstream into the mammary secretion of goats during pregnancy but not lactation; higher concentrations were observed in milk fractions derived from the alveoli than from the ducts, indicating that most of the leaky tight junctions are in the alveolar epithelium.…”

Section: Introductionsupporting

confidence: 83%

Hormonal regulation of tight junction closure in the mouse mammary epithelium during the transition from pregnancy to lactation

Da¹,

Af²,

Mc³

2001

Journal of Endocrinology

160

127

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Closure of the tight junctions of the mammary epithelium has been shown to accompany the onset of copious milk secretion or lactogenesis, stage 2, in both goats and humans. Here we use injection of [ 14 C]sucrose and FITC-albumin (fluorescein isothiocyanate-albumin) into the mammary duct to follow the course of tight junction closure during lactogenesis in mice. To examine the hormonal changes responsible, we ovariectomized day 16 or 17 pregnant mice and found that closure followed ovariectomy with a mean delay of 13·6 1·5 (...) h. That progesterone withdrawal is the trigger for closure was shown by the finding that injection of progesterone within 4 h of ovariectomy delayed closure and that closure occurred after injection of the progesterone antagonist RU 486 in intact late pregnant mice. Endocrine ablation studies showed that low to moderate concentrations of corticosterone and either placental lactogen or prolactin are necessary for tight junction closure triggered by progesterone withdrawal. Thus the hormonal requirements for tight junction closure are similar to those shown by other investigators to promote lactogenesis, stage 2. Further, the tight temporal control of tight junction permeability suggests that ovariectomy of the late pregnant mouse may be a good model for molecular studies of the lactogenic switch.

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“…Hartmann and others noted that the initiation of lactation took place in two stages [29]. The first stage occurred during late pregnancy when variable amounts of lactose could be observed in the mammary gland of the cow; he called this stage "lactogenesis I" [30]. We now call it secretory differentiation.…”

Section: Alveolar Differentiation and Secretory Activationmentioning

confidence: 96%

“…In pregnancy the mammary epithelium is extremely leaky such that proteins such as lactalbumin can pass from the lumen to the blood stream and blood proteins can enter the milk space [36]. During lactation the epithelium is among the tightest known, actually maintaining a potential difference up to -35 mV [30]. The switch between the two states was studied simultaneously in the early 1970's by Linzell and Peaker at Babraham and Dorothy Pitelka at Berkeley.…”

Section: Alveolar Differentiation and Secretory Activationmentioning

confidence: 99%

Classic Studies of Mammary Development and Milk Secretion: 1945 – 1980

Neville¹

2009

J Mammary Gland Biol Neoplasia

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On June 20, 1947 a meeting at the Royal Society of Medicine in London was entitled "Discussion on Some Recent Developments in Knowledge of the Physiology of the Breast" [1]. The major questions outlined by the speakers were: how does the structure of the breast change with reproductive stage? what is the role of the basal cell layer in the mammary epithelium? how is milk composition related to diet? and what is the basic physiology of milk secretion including its hormonal regulation? All these questions were attacked vigorously in laboratories mostly in England and the United States, but researchers in France, Germany, and Austria also weighed in. Our purpose in this edition of the Journal is to show, through the presentation of seminal papers and key references, how the research of that period, prior to the molecular revolution of the last three decades, laid the groundwork for our current understanding of the morphology, developmental biology, and physiology of the functional mammary gland. This knowledge provides the groundwork for our current research into the molecular mechanisms involved in milk secretion and its regulation.

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Electrical potentials and cell-to-cell dye movement in mouse mammary gland during lactation

Cited by 43 publications

References 24 publications

Induction of distinct types of spontaneous electrical activities in mammary epithelial cells by epidermal growth factor and insulin.

Induction of distinct types of spontaneous electrical activities in mammary epithelial cells by epidermal growth factor and insulin.

Hormonal regulation of tight junction closure in the mouse mammary epithelium during the transition from pregnancy to lactation

Classic Studies of Mammary Development and Milk Secretion: 1945 – 1980

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