GABAergic synaptic scaling in embryonic motoneurons is mediated by a shift in the chloride reversal potential

• Type of Material: Article
• Authors: Carlos E Gonzalez Islas, Emory University; Nikolai Chub, National Institutes of Health; Miguel Angel Garcia-Bereguiain, Emory University; Peter Wenner, Emory University
• Language: English
• Date: 2010-09-29
• Publisher: Society for Neuroscience
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © 2010 the authors
• Final Published Version (URL): http://dx.crossref.org/10.1523/JNEUROSCI.1659-10.2010
• Title of Journal or Parent Work: Journal of Neuroscience Nursing
• ISSN: 0270-6474
• Volume: 30
• Issue: 39
• Start Page: 13016
• End Page: 13020
• Grant/Funding Information: This research was supported by National Institute of Neurological Disorders and Stroke Grant NS046510 and National Science Foundation Grant 0616097 to P.W. and by the Intramural Program of the National Institutes of Neurological Disorders and Stroke. We thank Drs. Michael O'Donovan and Mark Rich for their comments on the manuscript, and Dr. Porfirio Nava for assistance with Western blots.
• Keywords: synaptic plasticity; spinal cord; motoneuron; GABAA receptor; GABA; development
• Research Categories: Biology, Neuroscience

Abstract

Homeostatic synaptic plasticity ensures that networks maintain specific levels of activity by regulating synaptic strength in a compensatory manner. When spontaneous network activity (SNA) was blocked in vivo in the embryonic spinal cord, compensatory increases in excitatory GABAergic synaptic inputs were observed. This homeostatic synaptic strengthening was observed as an increase in the amplitude of GABAergic miniature postsynaptic currents (mPSCs). We find that this process is mediated by an increase in chloride accumulation which produces a depolarizing shift in the GABAergic reversal potential (EGABA). The findings demonstrate a previously unrecognized mechanism underlying homeostatic synaptic scaling. Similar shifts in EGABA have been described following various forms of neuronal injury, introducing the possibility that these shifts in EGABA represent a homeostatic response.