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dc.contributor.authorVega-Vela N.E.
dc.contributor.authorOsorio D.
dc.contributor.authorAvila-Rodriguez M.
dc.contributor.authorGonzalez J.
dc.contributor.authorGarcía-Segura L.M.
dc.contributor.authorEcheverria V.
dc.contributor.authorBarreto G.E.
dc.date.accessioned2020-09-02T22:29:57Z
dc.date.available2020-09-02T22:29:57Z
dc.date.issued2017
dc.identifier10.1007/s12035-016-0045-6
dc.identifier.citation54, 7, 4996-5007
dc.identifier.issn08937648
dc.identifier.urihttps://hdl.handle.net/20.500.12728/6529
dc.descriptionVoltage-gated calcium channels are key regulators of brain function, and their dysfunction has been associated with multiple conditions and neurodegenerative diseases because they couple membrane depolarization to the influx of calcium—and other processes such as gene expression—in excitable cells. L-type calcium channels, one of the three major classes and probably the best characterized of the voltage-gated calcium channels, act as an essential calcium binding proteins with a significant biological relevance. It is well known that estradiol can activate rapidly brain signaling pathways and modulatory/regulatory proteins through non-genomic (or non-transcriptional) mechanisms, which lead to an increase of intracellular calcium that activate multiple kinases and signaling cascades, in the same way as L-type calcium channels responses. In this context, estrogens—L-type calcium channels signaling raises intracellular calcium levels and activates the same signaling cascades in the brain probably through estrogen receptor-independent modulatory mechanisms. In this review, we discuss the available literature on this area, which seems to suggest that estradiol exerts dual effects/modulation on these channels in a concentration-dependent manner (as a potentiator of these channels in pM concentrations and as an inhibitor in nM concentrations). Indeed, estradiol may orchestrate multiple neurotrophic responses, which open a new avenue for the development of novel estrogen-based therapies to alleviate different neuropathologies. We also highlight that it is essential to determine through computational and/or experimental approaches the interaction between estradiol and L-type calcium channels to assist these developments, which is an interesting area of research that deserves a closer look in future biomedical research. © 2016, Springer Science+Business Media New York.
dc.language.isoen
dc.publisherHumana Press Inc.
dc.subjectCalcium signaling
dc.subjectDHP binding site
dc.subjectEstradiol
dc.subjectEstrogen non-genomic actions
dc.subjectEstrogen receptor-independent mechanisms
dc.subjectVoltage-gated calcium channels
dc.subjectcalcium
dc.subjectcalcium channel L type
dc.subjectestradiol
dc.subjectcalcium
dc.subjectcalcium channel L type
dc.subjectestradiol
dc.subjectestrogen
dc.subjectastrocyte
dc.subjectbiochemistry
dc.subjectbrain level
dc.subjectcalcium signaling
dc.subjectconcentration (parameters)
dc.subjecthormone action
dc.subjecthuman
dc.subjectprotein binding
dc.subjectprotein expression
dc.subjectprotein function
dc.subjectprotein localization
dc.subjectReview
dc.subjectsignal transduction
dc.subjectanimal
dc.subjectdrug effect
dc.subjectmetabolism
dc.subjectnerve cell
dc.subjectAnimals
dc.subjectCalcium
dc.subjectCalcium Channels, L-Type
dc.subjectEstradiol
dc.subjectEstrogens
dc.subjectHumans
dc.subjectNeurons
dc.subjectSignal Transduction
dc.titleL-Type Calcium Channels Modulation by Estradiol
dc.typeReview


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