Homeostatic Intrinsic Plasticity Is Functionally Altered in Fmr1 KO Cortical Neurons

• Type of Material: Article
• Authors: Pernille Bulow, Emory University; Thomas Murphy, Emory University; Gary Bassell, Emory University; Peter Wenner, Emory University
• Language: English
• Date: 2019-02-05
• Publisher: CELL PRESS
• Publication Version: Final Published Version
• Copyright Statement: © 2019 The Author(s)
• License: Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International
• Final Published Version (URL): http://dx.doi.org/10.1016/j.celrep.2019.01.035
• Title of Journal or Parent Work: Cell Reports
• Volume: 26
• Issue: 6
• Start Page: 1378
• End Page: +
• Grant/Funding Information: This work was supported by grants R01MH109026 from the National Institute of Mental Health (G.J.B.) and R01NS065992 from the National Institute of Neurological Disorders and Stroke (P.W.).
• Keywords: Life Sciences & Biomedicine; Science & Technology; Cell Biology; HYPEREXCITABILITY; EXCITABILITY; MENTAL-RETARDATION PROTEIN; MOUSE MODEL; TRANSMISSION; EXPRESSION; COMPENSATION; MESSENGER-RNAS; TRANSLATION; SYNAPTIC PLASTICITY
• Research Categories: Health Sciences, Pharmacology; Biology, Cell; Biology, Physiology

Abstract

Fragile X syndrome (FXS) is characterized by cortical hyperexcitability, but the mechanisms driving hyperexcitability are poorly understood. Homeostatic intrinsic plasticity (HIP) regulates ion channel function to maintain appropriate activity levels. Bülow et al. show that HIP is functionally altered in FXS neurons, which may leave cortical neurons vulnerable to hyperexcitability.