Frontiers in Cellular Neuroscience Cellular Neuroscience

Abstract

using pharmacological manipulations of GABA signaling, such as fluoxetine, to reinstate ocular dominance plasticity in adult visual cortex and facilitate recovery from amblyopia (Maya Vetencourt et al., 2008; Harauzov et al., 2010). Taken together, these studies are providing a better understanding for the role of GABAergic signaling in the maturation and function of the visual cortex, and have opened the door for the development of new treatments for neurodevelopmental disorders such as amblyopia. The GABAergic synapse is a complex structure with a large set of pre-and post-synaptic proteins, many of which have been linked with experience-dependent plasticity in the cortex. On the pre-syn-aptic side these include: the two isoforms of the GABA synthesizing enzyme glutamic acid decarboxylase (GAD), GAD65 and GAD67; the CB1 receptor that modulates GABA release; and the vesicular transporter VGAT that is responsible for loading GABA into syn-aptic vesicles (McIntire et al., 1997; Sagne et al., 1997). GAD65 is localized in the axon terminals and synthesizes the on-demand pool of GABA, while GAD67 is located in the cell body and synthesizes the basal pool of GABA (Feldblum et al., 1993, 1995). Knocking out GAD65 leads to a loss of critical period ocular dominance plasticity, however, it can be rescued by infusion of diazepam (Iwai et al., 2003). Activation of CB1 receptors is involved in regulating activity-dependent synaptic plasticity (Sjöström et al., 2003; Jiang