Abstract

Experience is required for the shaping and refinement of developing neural circuits during well defined periods of early postnatal development called critical periods. Many studies in the visual cortex have shown that intracortical GABAergic circuitry plays a crucial role in defining the time course of the critical period for ocular dominance plasticity. With the end of the critical period, neural plasticity wanes and recovery from the effects of visual defects on visual acuity (amblyopia) or binocularity is much reduced or absent. Recent results pointed out that intracortical inhibition is a fundamental limiting factor for adult cortical plasticity and that its reduction by means of different pharmacological and environmental strategies makes it possible to greatly enhance plasticity in the adult visual cortex, promoting ocular dominance plasticity and recovery from amblyopia. Here we focus on the role of intracortical GABAergic circuitry in controlling both developmental and adult cortical plasticity. We shall also discuss the potential clinical application of these findings to neurological disorders in which synaptic plasticity is compromised because of excessive intracortical inhibition.

Highlights

  • What we are, how we behave, how we talk, how we perceive, crucially depends upon how our brain has developed

  • As experience drives the remodeling of neural connections, determining the maturation of neural circuits and of the corresponding functions, both circuits and functions become progressively less modifiable by experience and critical periods (CPs) draw towards their closure

  • In these mice BDNF expression in the visual cortex is higher than in wt mice starting from very early postnatal ages and this correlates with a precocious development of Intracortical GABAergic inhibition (IGI), as shown by the faster developmental increase in inhibitory postsynaptic currents and GABA biosynthetic enzyme GAD65 in the perisomatic region of pyramidal cells

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Summary

GABAergic inhibition in visual cortical plasticity

Alessandro Sale1*†, Nicoletta Berardi1,2†, Maria Spolidoro, Laura Baroncelli and Lamberto Maffei. Edited by: Yehezkel Ben-Ari, Institut National de la Santé et de la Recherche Médicale, France. Reviewed by: Rustem Khazipov, Institut National de la Santé et de la Recherche Médicale, France Evelyne Sernagor, Newcastle University, UK. Many studies in the visual cortex have shown that intracortical GABAergic circuitry plays a crucial role in defining the time course of the critical period for ocular dominance plasticity. With the end of the critical period, neural plasticity wanes and recovery from the effects of visual defects on visual acuity (amblyopia) or binocularity is much reduced or absent. Recent results pointed out that intracortical inhibition is a fundamental limiting factor for adult cortical plasticity and that its reduction by means of different pharmacological and environmental strategies makes it possible to greatly enhance plasticity in the adult visual cortex, promoting ocular dominance plasticity and recovery from amblyopia.

INTRODUCTION
GABA and visual cortex plasticity
Full Text
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