Neuronal chloride and excitability - the big impact of small changes.

Joseph V Raimondo, Blake A Richards, Melanie A Woodin

Journal: Current opinion in neurobiology 2018;43():35-42

PMID: 27992777

Full Text on Elsevier Science View on PubMed

Abstract

Synaptic inhibition is a critical regulator of neuronal excitability, and in the mature brain the majority of synaptic inhibition is mediated by Cl-permeable GABA receptors. Unlike other physiologically relevant ions, Cl is dynamically regulated, and alterations in the Cl gradient can have significant impact on neuronal excitability. Due to changes in the neuronal Cl concentration, GABAergic transmission can bidirectionally regulate the induction of excitatory synaptic plasticity and gate the closing of the critical period for monocular deprivation in visual cortex. GABAergic circuitry can also provide a powerful restraining mechanism for the spread of excitation, however Cl extrusion mechanisms can become overwhelmed and GABA can paradoxically contribute to pathological excitation such as the propagation of seizure activity.

Address: Division of Physiology, Department of Human Biology and Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Anzio Road Observatory, 7925 Cape Town, South Africa.; Department of Biological Sciences, University of Toronto Scarborough, 1265 Military Trail, Toronto, Ontario M1C 1A4, Canada; Department of Cell and Systems Biology, University of Toronto, 25 Harbord Street, Toronto, Ontario M5S 3G5, Canada.; Department of Cell and Systems Biology, University of Toronto, 25 Harbord Street, Toronto, Ontario M5S 3G5, Canada. Electronic address: [email protected].

DOI: 10.1016/j.conb.2016.11.012

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MeSH Terms: Chlorides, Humans, Neuronal Plasticity, Neurons, Receptors, GABA-A, Visual Cortex