, 1999, Antonini and Stryker, 1996 and Shatz and Stryker, 1978) and intracortical (Schmidt et al., 1997 and Trachtenberg and Stryker, 2001) projections. These changes in axonal organization are matched by structural
plasticity of dendritic spines which accommodate most excitatory synapses. This is evident from a temporary reduction in spine density of layer 3 pyramidal neurons after several days of MD (Mataga et al., 2004). Using two-photon microscopy it was shown that many spines are continuously being replaced in the neocortex and that this turnover steeply increases during the induction of plasticity (Grutzendler et al., 2002, Hofer et al., 2009, Lendvai et al., 2000 and Trachtenberg et al., Metabolism inhibitor 2002). This turnover declines with age (Holtmaat et al., 2005). In adult mice, the percentage of persistent spines increases and the reorganization of thalamocortical projections becomes limited (Antonini et al., 1999 and Holtmaat et al., 2005). While OD plasticity in adulthood is associated with increased spine dynamics in layer 5 pyramidal neurons this is not observed in layer 3 pyramidal neurons (Hofer et al., 2009). Also, the spine loss observed in layer 3 pyramidal neurons after MD during Selleckchem Rapamycin the critical period is not detected in adulthood (Mataga et al., 2004). Interestingly, a large shift in OD plasticity can still be induced in these neurons (Hofer et al., 2009) suggesting
that other plasticity mechanisms may become dominant in adult V1. One such mechanism could be the structural plasticity of inhibitory inputs onto these pyramidal neurons. Whole-cell recordings in vitro and in vivo suggest that inhibitory innervation of excitatory neurons is altered by MD (Maffei et al., 2006 and Yazaki-Sugiyama et al., 2009) and some evidence supports the idea that in the adult visual oxyclozanide cortex, interneurons retain higher plasticity levels than excitatory neurons (Chen et al., 2011, Kameyama et al., 2010 and Lee et al., 2006). It was recently shown that presynaptic boutons of subsets of interneurons are lost rapidly upon retinal lesioning indicating that inhibitory synapses
have the potential to undergo structural plasticity in adult V1 (Keck et al., 2011). However, as the same paradigm also causes massive restructuring of excitatory synapses in adult V1 (Keck et al., 2008), the implications for deprivation-based paradigms such as OD plasticity are not clear. In this study we directly tested whether OD plasticity in the adult visual cortex is associated with structural plasticity of inhibitory synapses on layer 2/3 pyramidal neurons. We labeled their inhibitory synapses by electroporating the neurons in utero with a red fluorescent cytoplasmic protein together with green fluorescent protein (GFP)-tagged gephyrin, a scaffold protein specifically present in the inhibitory postsynapse (Kneussel et al., 2001 and Sassoè-Pognetto et al., 1999).