Neuronal chloride and excitability — the big impact of small changes

Publication date: April 2017
Source:Current Opinion in Neurobiology, Volume 43
Author(s): Joseph V Raimondo, Blake A Richards, Melanie A Woodin
Synaptic inhibition is a critical regulator of neuronal excitability, and in the mature brain the majority of synaptic inhibition is mediated by Cl⁻-permeable GABAA 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.



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