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Taguchi, Yasuto; Koslowski, Mirek; Bodenner, Donald

doi:10.1186/1478-1336-2-5

Cited by 73 publications

(28 citation statements)

References 31 publications

(29 reference statements)

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“…Mice receiving intracerebroventricular (ICV) injections of BSA-E 2 spent more time investigating a novel object compared to a familiar object, indicating memory of the familiar object [91]. Since BSA-E 2 is unable to cross the cell membrane [92], it can be inferred that the rapid effects of estradiol on object recognition depends on the activation of membrane-bound receptors, such as GPR30 [23, 93, 94]. These behavioral effects were not blocked by the nuclear ER agonist ICI 182,780, further supporting the hypothesized role of membrane-bound ERs in social [90] and non-social learning [91].…”

Section: Rapid Effects Of Estrogens On Behaviormentioning

confidence: 99%

Rapid effects of estrogens on behavior: Environmental modulation and molecular mechanisms

Laredo

Landeros

Trainor

2014

Frontiers in Neuroendocrinology

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Estradiol can modulate neural activity and behavior via both genomic and nongenomic mechanisms. Environmental cues have a major impact on the relative importance of these signaling pathways with significant consequences for behavior. First we consider how photoperiod modulates nongenomic estrogen signaling on behavior. Intriguingly, short days permit rapid effects of estrogens on aggression in both rodents and song sparrows. This highlights the importance of considering photoperiod as a variable in laboratory research. Next we review evidence for rapid effects of estradiol on ecologically-relevant behaviors including aggression, copulation, communication, and learning. We also address the impact of endocrine disruptors on estrogen signaling, such as those found in corncob bedding used in rodent research. Finally, we examine the biochemical mechanisms that may mediate rapid estrogen action on behavior in males and females. A common theme across these topics is that the effects of estrogens on social behaviors vary across different environmental conditions.

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Section: Rapid Effects Of Estrogens On Behaviormentioning

confidence: 99%

Rapid effects of estrogens on behavior: Environmental modulation and molecular mechanisms

Laredo

Landeros

Trainor

2014

Frontiers in Neuroendocrinology

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“…To address this issue, the current study employed two E2 conjugates, E2-BSA conjugate [30], [31], [32] and the newer E2 dendrimer conjugate (EDC) [33], which due to their size and charge cannot enter the cell nucleus. EDC and E2-BSA retain their ability to induce rapid extranuclear-mediated nongenomic signaling, but lack significant nuclear ER-mediated genomic signaling ability due to their inability to enter the cell nucleus and interact with nuclear ER [32], [33].…”

Section: Introductionmentioning

confidence: 99%

Extranuclear Estrogen Receptors Mediate the Neuroprotective Effects of Estrogen in the Rat Hippocampus

et al. 2010

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Background17β-estradiol (E2) has been implicated to exert neuroprotective effects in the brain following cerebral ischemia. Classically, E2 is thought to exert its effects via genomic signaling mediated by interaction with nuclear estrogen receptors. However, the role and contribution of extranuclear estrogen receptors (ER) is unclear and was the subject of the current study.Methodology/Principal FindingsTo accomplish this goal, we employed two E2 conjugates (E2 dendrimer, EDC, and E2-BSA) that can interact with extranuclear ER and exert rapid nongenomic signaling, but lack the ability to interact with nuclear ER due to their inability to enter the nucleus. EDC or E2-BSA (10 µM) was injected icv 60 min prior to global cerebral ischemia (GCI). FITC-tagged EDC or E2-BSA revealed high uptake in the hippocampal CA1 region after icv injection, with a membrane (extranuclear) localization pattern in cells. Both EDC and E2-BSA exerted robust neuroprotection in the CA1 against GCI, and the effect was blocked by the ER antagonist, ICI182,780. EDC and E2-BSA both rapidly enhanced activation of the prosurvival kinases, ERK and Akt, while attenuating activation of the proapoptotic kinase, JNK following GCI, effects that were blocked by ICI182,780. Administration of an MEK or PI3K inhibitor blocked the neuroprotective effects of EDC and E2-BSA. Further studies showed that EDC increased p-CREB and BDNF in the CA1 region in an ERK- and Akt-dependent manner, and that cognitive outcome after GCI was preserved by EDC in an ER-dependent manner.Conclusions/SignificanceIn conclusion, the current study demonstrates that activation of extranuclear ER results in induction of ERK-Akt-CREB-BDNF signaling in the hippocampal CA1 region, which significantly reduces ischemic neuronal injury and preserves cognitive function following GCI. The study adds to a growing literature that suggests that extranuclear ER can have important actions in the brain.

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“…BSA (6,(41)(42)(43)(44) or horseradish peroxidase (7,(45)(46). There is a large body of evidence in favor of the existence of plasma membrane receptors for 17␤-estradiol, and numerous such receptors have been proposed.…”

mentioning

confidence: 99%

17β-Estradiol Elevates cGMP and, via Plasma Membrane Recruitment of Protein Kinase GIα, Stimulates Ca2+ Efflux from Rat Hepatocytes

Stratton

Squires

Green

2010

Journal of Biological Chemistry

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Rapid non-genomic effects of 17␤-estradiol, the principal circulating estrogen, have been observed in a wide variety of cell types. Here we investigate rapid signaling effects of 17␤-estradiol in rat hepatocytes. We show that, above a threshold concentration of 1 nM, 17␤-estradiol, but not 17␣-estradiol, stimulates particulate guanylyl cyclase to elevate cGMP, which through activation and plasma membrane recruitment of protein kinase G isoform I␣, stimulates plasma membrane Ca 2؉ -ATPase-mediated Ca 2؉ efflux from rat hepatocytes. These effects are extremely rapid in onset and are mimicked by a membrane-impermeant 17␤-estradiol-BSA conjugate, suggesting that 17␤-estradiol acts at the extracellular face of the plasma membrane. We also show that 17␤-estradiol binds specifically to the intact hepatocyte plasma membrane through an interaction that is competed by an excess of atrial natriuretic peptide but also shows many similarities to the pharmacological characteristics of the putative ␥-adrenergic receptor. We, therefore, propose that the observed rapid signaling effects of 17␤-estradiol are mediated either through the guanylyl cyclase A receptor for atrial natriuretic peptide or through the ␥-adrenergic receptor, which is either itself a transmembrane guanylyl cyclase or activates a transmembrane guanylyl cyclase through cross-talk signaling.

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Untitled

Cited by 73 publications

References 31 publications

Rapid effects of estrogens on behavior: Environmental modulation and molecular mechanisms

Rapid effects of estrogens on behavior: Environmental modulation and molecular mechanisms

Extranuclear Estrogen Receptors Mediate the Neuroprotective Effects of Estrogen in the Rat Hippocampus

17β-Estradiol Elevates cGMP and, via Plasma Membrane Recruitment of Protein Kinase GIα, Stimulates Ca2+ Efflux from Rat Hepatocytes

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