Abstract
Cortical injuries are a leading cause of death and disability worldwide. The first weeks post-lesion are usually crucial to predict the final outcome of patients. While most of them experience a spontaneous, at least partial, restoration of function, in some the clinical picture is complicated due to the development of epileptic seizures. A substantial number of studies suggest that these phenomena may be triggered by complex functional alterations in intracortical inhibition, often observed in perilesional cortical areas. Pathophysiological changes in GABAergic transmission are indeed likely to alter plasticity, excitability, and function of cortical circuits. The development of more efficient therapeutic strategies may, therefore, require a deep understanding into lesion-induced changes in inhibition at both the cellular and neuronal network levels. In this review, we gather together information from recent studies which have focused on dissecting alterations at inhibitory synapses as well as in the function of different subclasses of interneurons following cortical lesions.
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Notes
EGABA is the neuronal membrane potential at which the net flow of GABAARs permeable ions (Cl− and to a minor extent HCO3 − ions), across a neuronal membrane, following receptor activation, is zero. At this specific potential the concentration gradient force to drive Cl− ions (and HCO3 −) into a neuron, is equal and, therefore, neutralized by the electrical force that drives negatively charged ions out of a negatively polarized neuron.
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Conflict of interest. B. Imbrosci and T. Mittmann have made no statement.
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Mittmann, T., Imbrosci, B. New insights into the role of GABAergic inhibition during functional reorganization of the visual cortex post-lesion. e-Neuroforum 5, 12–19 (2014). https://doi.org/10.1007/s13295-014-0052-x
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DOI: https://doi.org/10.1007/s13295-014-0052-x