ArticleMolecular pain2009
Glycine receptor in rat hippocampal and spinal cord neurons as a molecular target for rapid actions of 17-beta-estradiol.
Article in Molecular pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Human GlyRα2 pore dynamics in gating and inhibition.Structure (London, England : 1993) · 2026Article
- Pain mechanisms in the transgender individual: a review.Frontiers in pain research (Lausanne, Switzerland) · 2024Review
- Steroid Sulfation in Neurodegenerative Diseases.Frontiers in molecular biosciences · 2022Review
- Role of sex hormones in modulating breast and ovarian cancer associated pain.Molecular and cellular endocrinology · 2021Article
- Ethanol consumption and sedation are altered in mice lacking the glycine receptor α2 subunit.British journal of pharmacology · 2020Article
- Neurosteroids as Selective Inhibitors of Glycine Receptor Activity: Structure-Activity Relationship Study on Endogenous Androstanes and Androstenes.Frontiers in molecular neuroscience · 2020Article
- Glycine attenuates cerebrovascular remodeling via glycine receptor alpha 2 and vascular endothelial growth factor receptor 2 after stroke.American journal of translational research · 2020Article
- Calcium-engaged Mechanisms of Nongenomic Action of Neurosteroids.Current neuropharmacology · 2017Review
- Activation of glycine and extrasynaptic GABA(A) receptors by taurine on the substantia gelatinosa neurons of the trigeminal subnucleus caudalis.Neural plasticity · 2013Article
- Involvement of estrogen in rapid pain modulation in the rat spinal cord.Neurochemical research · 2012Article
- Estrogen facilitates spinal cord synaptic transmission via membrane-bound estrogen receptors: implications for pain hypersensitivity.The Journal of biological chemistry · 2012Article
- Mechanisms of G protein-coupled estrogen receptor-mediated spinal nociception.The journal of pain · 2012Article
- Rapid estrogenic effects on TMJ-responsive brainstem neurons.Journal of dental research · 2012Article
- Estrogen in cycling rats alters gene expression in the temporomandibular joint, trigeminal ganglia and trigeminal subnucleus caudalis/upper cervical cord junction.Journal of cellular physiology · 2011Article
- Potentiation of excitatory transmission in substantia gelatinosa neurons of rat spinal cord by inhibition of estrogen receptor alpha.Molecular pain · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycine receptors (GlyRs) play important roles in regulating hippocampal neural network activity and spinal nociception. Here we show that, in cultured rat hippocampal (HIP) and spinal dorsal horn (SDH) neurons, 17-beta-estradiol (E2) rapidly and reversibly reduced the peak amplitude of whole-cell glycine-activated currents (IGly). In outside-out membrane patches from HIP neurons devoid of nuclei, E2 similarly inhibited IGly, suggesting a non-genomic characteristic. Moreover, the E2 effect on IGly persisted in the presence of the calcium chelator BAPTA, the protein kinase inhibitor staurosporine, the classical ER (i.e. ERalpha and ERbeta) antagonist tamoxifen, or the G-protein modulators, favoring a direct action of E2 on GlyRs. In HEK293 cells expressing various combinations of GlyR subunits, E2 only affected the IGly in cells expressing alpha2, alpha2beta or alpha3beta subunits, suggesting that either alpha2-containing or alpha3beta-GlyRs mediate the E2 effect observed in neurons. Furthermore, E2 inhibited the GlyR-mediated tonic current in pyramidal neurons of HIP CA1 region, where abundant GlyR alpha2 subunit is expressed. We suggest that the neuronal GlyR is a novel molecular target of E2 which directly inhibits the function of GlyRs in the HIP and SDH regions. This finding may shed new light on premenstrual dysphoric disorder and the gender differences in pain sensation at the CNS level.
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