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PubMed1990

The effect of cortisol administration on hepatic and plasma estradiol-binding capacity in immature female rainbow trout (Oncorhynchus mykiss).

Implantation of a cortisol-containing pellet into the peritoneal cavity of immature female rainbow trout raised plasma cortisol levels within the range commonly observed in chronically stressed fish. In cortisol-implanted fish there was a significant decline in the concentration of hepatic estradiol-binding sites relative to sham-implanted controls. This consisted of a 35% drop in cytosolic binding sites and a 29% reduction in the number of nuclear estradiol-binding sites, by 4 weeks postimplantation. Plasma estradiol-binding capacity was also influenced by cortisol treatment. After 2 weeks there was a 33% increase in plasma estradiol-binding capacity of cortisol-implanted fish. Plasma estradiol levels were unaffected by cortisol implantation, suggesting that the effects of cortisol on estradiol-binding sites were not mediated by altering the rate of estradiol secretion. The results indicate a possible mechanism by which environmental stress may suppress vitellogenesis.

Animals↗

PubMed1995

Physiological concentration of estradiol inhibits polymorphonuclear leukocyte chemotaxis via a receptor mediated system.

Estrogen exhibits a variety of actions, including immuno-modulatory effects, in vivo and in vitro. The mechanism by which estrogen exerts its anti-inflammatory effect is not yet understood. We investigated the possible mechanisms of estradiol acting via the polymorphonuclear leukocytes (PMNs), which are important in the immune response. The agent, 17 beta-estradiol, but not 17 alpha-estradiol, significantly reduced PMNs chemotaxis to FMLP in a dose-dependent manner (control vs estrogen 10(-10)-(-6) M, P < 0.05). Physiological concentrations of estradiol significantly reduced the chemotaxis of PMNs (10(-10) mol). Pre-incubation with clomiphene or tamoxifen which are estrogen receptor antagonists, eliminated the inhibitory effect of 17 beta-estradiol on the chemotaxis of PMNs, restoring it to the control level. These observations suggest that 17 beta-estradiol suppressed the chemotaxis of PMNs by a receptor-dependent mechanism. In addition, the level of estradiol in human plasma, which PMNs were drawn, showed a close, inverse correlation with the PMNs chemotaxis to FMLP (r = -0.821 p < 0.001). Estrogen may modify the activity of neutrophils during the normal menstrual cycle, not only during pregnancy, and influence inflammation.

Adult↗

PubMed1981

The aging Leydig cell: VII. Cytoplasmic estradiol receptors.

Plasma estradiol and cytosolic estradiol receptor levels of testes were determined in a group of young (2-3 months) and old (24 months) Sprague-Dawley rats. Estradiol binding sites for the young rats averaged 5.6 +/- 0.3 fmol/mg protein (x +/- SE, n=12), which was comparable to that of the old rats, 5.7 +/- 0.3 fmol/mg protein (n=12). Using Scatchard analyses, the association constants at equilibrium of estradiol receptor binding of the old and young rats were the same, 6.1 x 10 10 M-1. Plasma estradiol levels were also similar in both groups-19.6 +/- 2.8 pg/ml (n=14) for the young and 19.2 +/- 2.6 pg/ml (n=10) for the old rats. Our results suggest that impaired testosterone biosynthesis in old rats was not due to elevated plasma estradiol levels or to differences in testicular estradiol receptor content.

Aging↗

PubMed1985

Alterations in the prolactin secretion in streptozotocin-induced diabetic rats. Correlation with pituitary and hypothalamus estradiol receptors.

The present study examined the effects of streptozotocin-induced diabetes on prolactin (Prl) secretion and its correlation with estrogen receptor levels in the anterior pituitary and hypothalamus. Prl was measured in adult ovariectomized rats and after estradiol treatment (10 micrograms estradiol benzoate (Eb) 48, 24 and 1 h before experiments) or acute TRH administration (4 micrograms/kg body weight). Substantial decreases in estradiol- and TRH-induced Prl release were observed in diabetic rats. Insulin therapy was able to restore this response. Measurement of nuclear estradiol receptors by exchange assay in the pituitary of Eb-treated rats revealed a significant reduction in receptor levels in the diabetic group and a restoration to normal values in insulin-treated diabetic rats. Similar results were obtained by measuring total pituitary receptor content (cytosolic plus nuclear receptors). No significant changes were observed in nuclear hypothalamic estradiol receptors. However, the number of total hypothalamic estradiol receptors was diminished in diabetic rats although the translocation was proportionally greater in these animals. These results indicate that the disrupted reproductive functions described in streptozotocin diabetic rats may be due, at least in part, to deficiencies in Prl secretion and pituitary estradiol action.

Animals↗

PubMed1992

Synergistic interaction of growth factors and albumin in regulating estradiol synthesis in breast cancer cells.

Estradiol 17 beta-hydroxysteroid dehydrogenase acts to convert estrone to the biologically active estrogen, estradiol, in breast tumors and MCF-7 breast cancer cells in vitro. In this study we have examined the ability of albumin to influence the effect of growth factors (insulin-like growth factor-I (IGF-I), epidermal growth factor (EGF), transforming growth factor-alpha (TGF alpha)) and cytokines (interleukin (IL)-1, IL-6) on estradiol 17 beta-hydroxysteroid dehydrogenase activity in MCF-7 cells. IGF-I (80 ng/ml) or albumin (30 micrograms/ml) stimulated estradiol 17 beta-hydroxysteroid dehydrogenase activity by 144% and 102% (p less than 0.01). The combination of IGF-I and albumin, however, produced a marked (704%) synergistic stimulation of estradiol 17 beta-hydroxysteroid dehydrogenase activity. EGF or TGF alpha failed to stimulate estradiol 17 beta-hydroxysteroid dehydrogenase activity and no synergism with albumin was detected. IL-1 (10 ng/ml), but not IL-6, also stimulated estradiol 17 beta-hydroxysteroid dehydrogenase activity and acted synergistically with albumin to stimulate enzyme activity. MCF-7 cells were shown to specifically bind 125I-albumin and binding is increased by pretreatment of cells with IGF-I (80 ng/ml) for 48 h. It is concluded that the synergism that results from treating MCF-7 cells with albumin and IGF-I may result from increased albumin uptake and subsequent biological effect.

Albumins↗

PubMed1998

Thalidomide does not alter the pharmacokinetics of ethinyl estradiol and norethindrone.

OBJECTIVE: To evaluate the effect of thalidomide on the plasma pharmacokinetics of ethinyl estradiol (INN, ethinylestradiol) and norethindrone (INN, norethisterone). METHODS: Ten women who had undergone surgical sterilization were enrolled in an open-label crossover study conducted in the Georgetown University Clinical Research Center. The pharmacokinetics of single doses of 0.07 mg ethinyl estradiol and 2 mg norethindrone were measured at baseline and after 3 weeks of 200 mg thalidomide. Compliance with the thalidomide regimen was assessed with use of Medication Event Monitoring System (MEMS) caps. RESULTS: No changes were observed in the pharmacokinetics of ethinyl estradiol or norethindrone with thalidomide therapy. The mean +/- SD area under the plasma concentration-time curve (AUC0-infinity) for ethinyl estradiol was 6580 +/- 1100 ng.h/L at baseline and 5970 +/- 1560 ng.h/L after the thalidomide regimen (paired t test, P > .05). The values for norethindrone were 103 +/- 54 micrograms.h/L and 107 +/- 58 micrograms.h/L (paired t test, P > .05). No changes were observed for other pharmacokinetic parameters assessed for either ethinyl estradiol or norethindrone. No accumulation of thalidomide was seen after 21 days of therapy: day 1 AUC0-infinity 41.1 +/- 13.9 micrograms.h/mL; day 21 AUC0-infinity 59.6 +/- 27.3 micrograms.h/mL (paired t test, P > .05). No changes were observed for other pharmacokinetic parameters assessed for thalidomide between days 1 and 21. Thalidomide was well tolerated but caused variable degrees of sedation. The average thalidomide compliance rate was 97%. CONCLUSIONS: The pharmacokinetics of thalidomide do not change with 3 weeks of daily dosing. Thalidomide does not alter the pharmacokinetics of ethinyl estradiol or norethindrone. Therefore there is no drug interaction between thalidomide and these 2 drugs. The efficacy of oral contraceptives containing ethinyl estradiol and norethindrone should not be affected by concomitant thalidomide therapy.

Adult↗

PubMed1996

The pharmacodynamic effects of an oral contraceptive containing 3 mg micronized 17 beta-estradiol and 0.150 mg desogestrel for 21 days, followed by 0.030 mg desogestrel only for 7 days.

During oral treatment with 3 mg micronized 17 beta-estradiol and 0.150 mg desogestrel for 21 days followed by 0.030 mg (A) desogestrel (15 women) or placebo (B) (14 women) for 7 days, ovarian function, bleeding pattern and estradiol levels were evaluated. The study was performed in a group-comparative, double-blind fashion. During a pre-treatment control cycle, using ultrasound scan, follicular diameter was measured on cycle days 10-16 and endometrial thickness on one of cycle days 22-26. Estradiol was measured at the time of ultrasound scan and progesterone three times in the luteal phase. During three treatment cycles, follicular diameter and endometrial thickness were monitored three times weekly and at the same time, estradiol and progesterone were measured. Treatment resulted in anovulation in all women. Maximum and mean estradiol levels were approximately 900 pmol/l and 550 pmol/l during treatment, respectively, and approximately 200 pmol/l during the estradiol-free weeks in both groups. Ten women showed ovarian activity (follicle size > or = 15 mm) during treatment, seven in group A and three in group B. Endometrial thickness decreased approximately 3 mm during treatment in both groups. The incidence of breakthrough bleeding and spotting was higher in group A when compared to group B. The study indicates that the combination of 3.0 mg micronized estradiol and 0.150 mg desogestrel is an effective and safe contraceptive, offering an acceptable cycle control. The addition of a low dose of desogestrel during the pill-free period did not further suppress ovarian activity nor improve the bleeding pattern. The results of this study should be interpreted with great care, since the number of women studied is relatively small.

Adult↗

PubMed2002

Effects of testosterone and 17-beta-estradiol on TNF-alpha-induced E-selectin and VCAM-1 expression in endothelial cells. Analysis of the underlying receptor pathways.

This study investigated the effects of testosterone and 17-beta-estradiol on tumor necrosis factor-alpha (TNF-alpha)-induced endothelial expression of E-selectin and vascular cell adhesion molecule-1 (VCAM-1) and the potential roles of hormone receptors involved in these actions. Human umbilical vein endothelial cells (HUVEC) were stimulated with TNF-alpha in the presence or absence of testosterone or 17-beta-estradiol, and the expression of E-selectin and VCAM-1 was investigated. As shown by Western blot analysis, co-administration with testosterone or 17-beta-estradiol increased the expression of E-selectin and VCAM-1 induced by TNF-alpha at 6 h and 3 h, respectively. Similarly, RT-PCR analysis revealed a significant increase in the amount of mRNA for E-selectin and VCAM-1 after co-administration with testosterone or 17-beta-estradiol in TNF-alpha-stimulated HUVEC. The presence of mRNA and proteins for androgen receptor and estrogen receptor alpha in HUVEC was verified by RT-PCR and Western blot. Flow cytometric analysis showed that preincubation with androgen receptor antagonist cyproterone and estrogen receptor antagonist tamoxifen completely abrogated the upregulating effects of testosterone and 17-beta-estradiol on TNF-alpha-induced E-selectin and VCAM-1 expression, respectively. Expression of TNF receptors in TNF-alpha-stimulated HUVEC was not influenced by testosterone and 17-beta-estradiol. The data indicate that both testosterone and 17-beta-estradiol increase TNF-alpha-induced E-selectin and VCAM-1 expression in endothelial cells via a receptor-mediated system, and expression of TNF receptors are not changed in these actions. The implications of these results for the facilitory effects of both sex hormones on immune reactions are discussed.

Androgen Receptor Antagonists↗

PubMed1996

The structure of a complex of human 17beta-hydroxysteroid dehydrogenase with estradiol and NADP+ identifies two principal targets for the design of inhibitors.

BACKGROUND: The steroid hormone 17beta-estradiol is important in the genesis and development of human breast cancer. Its intracellular concentration is regulated by 17beta-hydroxysteroid dehydrogenase, which catalyzes the reversible reduction of estrone to 17beta-estradiol. This enzyme is thus an important target for inhibitor design. The precise localization and orientation of the substrate and cofactor in the active site is of paramount importance for the design of such inhibitors, and for an understanding of the catalytic mechanism. RESULTS: The structure of recombinant human 17beta-hydroxysteroid dehydrogenase of type 1 (17beta-HSD1) in complex with estradiol at room temperature has been determined at 1.7 A resolution, and a ternary 17betaHSD1-estradiol-NADP+ complex at -150 degrees C has been solved and refined at 2.20 A resolution. The structures show that estradiol interacts with the enzyme through three hydrogen bonds (involving side chains of Ser142, Tyr155 and His221), and hydrophobic interactions between the core of the steroid and nine other residues. The NADP+ molecule binds in an extended conformation, with the nicotinamide ring close to the estradiol molecule. CONCLUSIONS: From the structure of the complex of the enzyme with the substrate and cofactor of the oxidation reaction, the orientation of the substrates for the reduction reaction can be deduced with confidence. A triangular hydrogen-bond network between Tyr155, Ser142 and O17 from estradiol probably facilitates the deprotonation of the reactive tyrosine, while the conserved Lys159 appears not to be directly involved in catalysis. Both the steroid-binding site and the NADPH-binding site can be proposed as targets for the design of inhibitors.

Amino Acid Sequence↗

PubMed1986

The biochemical mechanisms of the stimulating action of estradiol on the growth of mammary tumours.

The mechanisms of stimulating effect of estradiol on the growth of hormone-dependent mammary tumours in experimental animals were studied. Estradiol receptors were detected in plasmatic membranes of estradiol-dependent tumour cells. Estradiol-independence of tumours was found to be a result of the impairment of the estradiol receptors in the plasmatic membranes, intracellular receptors, or of their ability to interact with the chromatin of the target cells. It was shown that the interaction of receptors of plasmatic membranes of hormone-dependent tumour cells with estradiol results in activation of the membrane adenylate cyclase and in a short-term rise of a cAMP content. A treatment of the hormone-dependent tumours with ovarian hormones brings about an increase in the activity of the cAMP-dependent protein kinases in cell nuclei, which points to their translocation from cytosol. Under effect of estradiol the phosphorylation of nuclear proteins at the serine, threonine and tyrosine residues increases.

Animals↗

PubMed1982

Translocation of the testicular estradiol receptor is not an obligatory step in the gonadotropin-induced inhibition of C17-20-lyase.

We have investigated the effects of hCG and estradiol on the time course of the inhibition of C17-20-lyase and the depletion of the estradiol cytosol receptor in testicular tissue of male rats. In hCG-treated animals the first significant decrease in C17-20-lyase activity was observed 16 h after injection of the hormone. The C17-20-lyase activity decreased further during the following 56 hours. Estradiol-cytosol receptor levels were significantly decreased 7 hours after the hCG injection, and after a nadir at 16 hours increased to 130% of control values at 72 hours. In contrast, in the estradiol-treated animals the first significant inhibition of C17-20-lyase activity could be observed only after 24 h, while a 95% depletion of estradiol-cytosol receptor levels was observed already within 1 h after administration of the hormone. These results demonstrate that a rapid estradiol-induced depletion of the estradiol receptor as such does not necessarily result in a subsequent immediate inhibition of the C17-20-lyase. The rapid inhibition of this enzyme after hCG indicates, therefore, that other mechanisms are involved.

Aldehyde-Lyases↗

PubMed1983

Estradiol and tamoxifen interaction at receptor sites at 37 C.

Mature rat uterine cytosol was pretreated with dextran-coated charcoal at 0 C for 2 h. This renders the subsequently formed estradiol-receptor complex thermostable at 37 C and also uncovers antiestrogen binding sites, possibly by removing an endogenous ligand. A sharp distinction is found between tamoxifen and estradiol as receptor ligands in pretreated cytosols in that tamoxifen will inhibit estradiol binding, on incubation at 37 C, only if dithiothreitol (DTT) had been included in the pretreatment solution. The presence of tamoxifen as the sole ligand in cytosol pretreated in the presence of DTT does not protect the estradiol receptor from thermal inactivation and following 37 C incubation tamoxifen is found bound exclusively to antiestrogen binding sites. Incubating the cytosol at 37 C with an equimolar mixture of estradiol and tamoxifen results in a very large increase in receptor-bound estradiol. This effect is attributed to the presence of tamoxifen complexed with antiestrogen sites. Tamoxifen in such equimolar ligand mixture binds to antiestrogen sites and is excluded from receptor sites by the estradiol, whose affinity for these sites is much greater than that of tamoxifen.

Animals↗

PubMed2004

Endogenous estradiol metabolism during treatment with oral contraceptives.

OBJECTIVE: Recent clinical studies indicate that an increase in D-ring estradiol metabolites over A-ring metabolites may be a risk factor for breast cancer. The present work was aimed to investigate the effect of oral contraceptives (OC) on the endogenous estradiol metabolism in premenopausal women. METHODS: Two studies were conducted, firstly comparing 2 different progestins, i.e. norethisterone and dienogest, each in combination with a constant ethinyl estradiol dosage (study A) and secondly comparing a single progestin, i.e. levonorgestrel in 2 ethinyl estradiol/progestin dosage combinations (study B). The main A- and D-ring metabolites, i.e. 2-OHE1 and 16-OHE1, were measured by enzyme immunoassay in 8-h night-urine collected before and after 3 cycles of OC administration. RESULTS: In study A, i.e. ethinyl estradiol plus dienogest or norethisterone acetate, the ratios of 16-OHE1 to 2-OHE1 before administration were 0.62 and 0.68, and after 3 months 0.31 and 0.54, respectively. The ratio after ethinyl estradiol and dienogest was significantly lower after treatment. In study B, i.e. ethinyl estradiol plus levonorgestrel (0.03 mg/0.15 mg and 0.02 mg/0.1 mg), the ratios before treatment were 0.71 and 0.75 for the higher and the lower dosages, respectively, which changed not significantly to 0.73 and 0.71 after 3 cycles. CONCLUSION: OCs containing norethisterone acetate, dienogest or levonorgestrel did not have a negative effect on estradiol metabolism, i.e. they did not elicit a higher D-ring metabolism, which is considered to increase breast cancer risk.

Adult↗

PubMedDate not supplied

[Sex hormone regulation of progesterone and estradiol receptors in the cytosol of human endometrium in normal and pathologic pregnancy].

Hormonal control of progesterone and estradiol receptors was studied in the cytozol of short-lived culture of human endometrium in normal and undeveloping pregnancy. Endometrium was cultivated in the presence of estradiol or progesterone for 16 hours. In cultivation of normal endometrium with estradiol the content of estradiol receptors increased 4-fold in comparison with unstimulated tissue, and of progesteron receptors--3-fold. In cultivation of normal endometrium with progesterone the content of estradiol receptors rose 4--5-fold, and of progesterone receptors--3-fold. In cultivation of pathological endometrium with estradiol or progesterone the number of estradiol receptors was only doubled, and of progesterone receptors--increased only 1 1/2 times, this pointing to a diminished sensitivity of pathological endometrium to the regulating action of sex hormones.

Cells, Cultured↗

PubMed1983

[Concentrations of estradiol in the quail magnum during sexual development. Relation to the levels of cytoplasmic receptors for this hormone].

Estradiol 17 beta concentration and cytoplasmic estradiol binding sites were determined in the magnum of immature and developing female Quail. In the immature magnum, estradiol concentration per gram of tissue was 26 times higher than in the plasma. Early sexual development was correlated with an increase in plasma and magnum concentrations of estradiol and of cytoplasmic binding sites in the magnum. However, the ratio of binding sites concentration to that of intra-tissue of estradiol, and the intracellular distribution of estradiol (cytoplasm versus nucleus) were similar in immature and developing Quail. The results indicate that the presence of estradiol and of binding sites in the target cells of the magnum are not sufficient to induce cell proliferation.

Animals↗

PubMed1984

Estradiol and progesterone receptors in malignant gastrointestinal tumors.

Estradiol and progesterone receptors were assayed in tumors from 79 patients with primary colorectal and 56 patients with stomach adenocarcinomas. Eighteen of 79 colorectal cancers contained estradiol receptor, while 34 specimens were positive for progesterone receptor. In stomach cancer, the positive samples were 8 for estradiol and 14 for progesterone receptors. In both types of tumors, the Kd was in the range of 10(-10) M for estradiol and 10(-9) M for progesterone receptor, respectively. In colorectal adenocarcinomas, the presence of progesterone receptor seems to be partially correlated to the presence of estradiol receptor while, in stomach tumors, this correlation is lost. The positivity of at least one receptor in colorectal cancers is higher in the female sex. The contrary occurs for stomach cancer. Sucrose gradient centrifugation showed that cytoplasmic estradiol receptor of stomach cancer sedimented at 8S or 4 to 5S at low ionic strength. The isoelectric point of stomach cancer estradiol receptor is 6.5.

Adenocarcinoma↗

PubMed2002

Estradiol administration improves splanchnic perfusion following trauma-hemorrhage and sepsis.

HYPOTHESIS: The female sex steroid 17beta-estradiol improves immune functions following trauma-hemorrhage in rodent models. Therefore, we hypothesized that 17beta-estradiol administration following trauma-hemorrhage would also improve cardiac output, splanchnic perfusion, and oxygen utilization, even after the induction of subsequent sepsis. SETTING: A university laboratory. INTERVENTION: Male rats underwent midline laparotomy (ie, soft tissue injury). They were bled to a mean arterial pressure of 35 to 40 mm Hg for 90 minutes and resuscitated over 60 minutes with lactated Ringer solution. At the beginning of resuscitation, 17beta-estradiol (l mg/kg) or a vehicle was administered. At 20 hours after resuscitation, polymicrobial sepsis was induced by cecal ligation and puncture (CLP). MAIN OUTCOME MEASURES: At 5 hours after CLP, cardiac performance (via a left ventricular catheter), cardiac output, and organ blood flow were determined using strontium 85 microspheres. Blood samples were collected from the femoral artery and jugular, portal, and renal veins to determine systemic and regional oxygen delivery and consumption. Moreover, circulating levels of 17beta-estradiol, its adrenal precursor dehydroepiandrosterone (DHEA), and corticosterone were assessed by enzyme-linked immunosorbent assay. RESULTS: Hemorrhage and subsequent sepsis significantly depressed cardiac performance, cardiac output, organ perfusion, and oxygen consumption. Estrogen did not restore cardiac output or systemic oxygen consumption; nonetheless, it restored the depressed intestinal perfusion. Rats treated with estrogen had significantly elevated levels of plasma 17beta-estradiol, but the levels of DHEA or corticosterone were not affected. CONCLUSIONS: The increase in gut perfusion could represent a potential mechanism for the salutary effects of 17beta-estradiol following trauma-hemorrhage. Because 17beta-estradiol improves systemic and intestinal perfusion after trauma-hemorrhage and induction of subsequent sepsis, this agent appears to be a promising adjunct for the treatment of trauma victims.

Animals↗

PubMed1996

Estradiol increases the frequency of multiple synapse boutons in the hippocampal CA1 region of the adult female rat.

The effect of estradiol to increase the density of dendritic spines and axospinous synapses on hippocampal CA1 pyramidal cells in the adult female rat has been well-documented. However, presynaptic involvement in this process of synapse elimination and formation in the adult is unknown. To address this issue, we have reconstructed 410 complete presynaptic boutons through coded serial electron micrographs of CA1 stratum radiatum to determine the: (1) frequency of multiple (MSB) vs. single (SSB) synapse boutons; (2) number of synaptic contacts per MSB; (3) bouton volume and surface area; and (4) types of spines in synaptic contact with MSBs and SSBs in ovariectomized, estradiol-treated animals (OVX + E) versus ovariectomized oil-treated controls (OVX + O). Quantitative analysis of this tissue revealed that, in OVX + E animals, 45.0% of presynaptic boutons form multiple synaptic contacts with dendritic spines compared to 27.3% in controls (P < 0.01); the average number of synapses per dendritic spines compared to 27.3% in controls (P < 0.01); the average number of synapses per MSB was 2.7 in OVX + E animals compared to 2.3 in controls (P < 0.05). This represents a 25.5% increase in the number of synapses formed by a given number of presynaptic boutons in estradiol-treated animals (P < 0.01) which largely accounts for the previously observed estradiol-induced increase in axospinous synapse density. There was no treatment effect on bouton size; however, because MSBs are larger than SSBs, the increased frequency of MSBs in estradiol-treated tissue results in a trend toward an estradiol-induced increase in average bouton size. Additionally, MSBS were found to be more irregular in shape, i.e., significantly less spherical, than SSBs. Our results indicate that estradiol-induced dendritic spines form synapses primarily with preexisting boutons in stratum radiatum and that these boutons enlarge and change shape as they accommodate new synapses. Such findings suggest a relatively active role for dendrites in the process of adult synapse formation.

Animals↗