Sex Differences in the Brain: The Estrogen Quandary

A special issue of Brain Sciences (ISSN 2076-3425). This special issue belongs to the section "Behavioral Neuroscience".

Deadline for manuscript submissions: closed (5 November 2019) | Viewed by 3966

Special Issue Editor


E-Mail Website
Guest Editor
Department of Biosciences and Nutrition, Karolinska Institutet, Huddinge, Sweden
Interests: estrogen; sex differences; neurodegeneration; neurodevelopment; sex hormones

Special Issue Information

Dear Colleagues,

Sex differences in the brain are established during important neurodevelopmental periods and are dependent on both genetic and hormonal factors. Such sex dimorphic imprinting is needed for normal physiology controlling reproduction and behavior. Its importance for brain function can be visualized by the sex differences in suceptibility to, and pathophysiology of, most neurodevelopmental and neurodegenerative diseases. Sex hormone signaling in the brain can impact on neurogenesis, neural migration, survival, synaptic plasticity, and axon guidance. Rodent models have shown estrogen in particular to be key in mediating these physiological mechanisms, as most testosterone is aromatized to estrogen in the rodent brain. However, the contribution of testosterone and estrogen in the human brain may be different, which warrants catious interpretation of rodent data and a need for more translational research. In addition, sex hormones signal in many ways. Estrogen may not only directly regulate gene transcription through binding to its receptors in the nuclus but can bind receptors in the cytoplasm or at the cell membrane to mediate fast nongenomic effects in different cell types in the brain. Thus, sex hormone signaling in the brain is very complex. Nevertheless, understanding how sex hormones contribute to brain development and function in males and females holds great promise to understand sex differences in neurological diseases and may lead to the discovery new treatments or preventive measures to combate these diseases.

The purpose of this Special Issue is to summarize the current knowledge on how sex hormones, in particular estrogen, contribute to sex differences in healthy and diseased brains. Furthermore, it will discuss how such knowledge can be used to find novel treatments for neurological diseases.

We look forward to your contributions.

Dr. Ivan Nalvarte
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Brain Sciences is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • sex differences
  • estrogen
  • neurobiology
  • sex hormones
  • brain

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

17 pages, 3824 KiB  
Article
Activation of Membrane Estrogen Receptors Attenuates NOP-Mediated Tactile Antihypersensitivity in a Rodent Model of Neuropathic Pain
by Danyeal M. Wright, Keri M. Small, Subodh Nag and Sukhbir S. Mokha
Brain Sci. 2019, 9(6), 147; https://doi.org/10.3390/brainsci9060147 - 21 Jun 2019
Cited by 6 | Viewed by 3687
Abstract
Women manifest a higher prevalence of several chronic pain disorders compared to men. We demonstrated earlier that estrogen rapidly attenuates nociceptin/orphanin FQ (N/OFQ) peptide receptor (NOP)-mediated thermal antinociception through the activation of membrane estrogen receptors (mERs). However, the effect of mER activation on [...] Read more.
Women manifest a higher prevalence of several chronic pain disorders compared to men. We demonstrated earlier that estrogen rapidly attenuates nociceptin/orphanin FQ (N/OFQ) peptide receptor (NOP)-mediated thermal antinociception through the activation of membrane estrogen receptors (mERs). However, the effect of mER activation on NOP-mediated attenuation of tactile hypersensitivity in a neuropathic model of pain and the underlying mechanisms remain unknown. Following spared nerve injury (SNI), male and ovariectomized (OVX) female rats were intrathecally (i.t.) injected with a selective mER agonist and nociceptin/orphanin FQ (N/OFQ), the endogenous ligand for NOP, and their effects on paw withdrawal thresholds (PWTs) were tested. In addition, spinal cord tissue was used to measure changes in phosphorylated extracellular signal regulated kinase (ERK), protein kinase A (PKA), protein kinase C (PKC), and protein kinase B (Akt) levels. SNI significantly reduced PWTs in males and OVX females, indicating tactile hypersensitivity. N/OFQ restored PWTs, indicating an antihypersensitive effect. Selective mER activation attenuated the effect of N/OFQ in an antagonist-reversible manner. SNI led to a robust increase in the phosphorylation of ERK, PKA, PKC, and Akt. However, mER activation did not further affect it. Thus, we conclude that activation of mERs rapidly abolishes NOP-mediated tactile antihypersensitivity following SNI via an ERK-, PKA-, PKC-, and Akt-independent mechanism. Full article
(This article belongs to the Special Issue Sex Differences in the Brain: The Estrogen Quandary)
Show Figures

Figure 1

Back to TopTop