Abstract
Inhibition from fast-spiking (FS) interneurons plays a crucial role in shaping cortical response properties and gating developmental periods of activity-dependent plasticity, yet the expression mechanisms underlying FS inhibitory plasticity remain largely unexplored. In layer 4 of visual cortex (V1), monocular deprivation (MD) induces either depression or potentiation of FS to star pyramidal neuron (FS→SP) synapses, depending on the age of onset (Maffei et al., 2004, 2006). This reversal in the sign (- to +) of plasticity occurs on the cusp of the canonical critical period (CP). To investigate the expression locus behind this switch in sign of inhibitory plasticity, mice underwent MD during the pre-CP [eye-opening to postnatal day (p)17] or CP (p22-p25), and FS→SP synaptic strength within layer 4 was assessed using confocal and immunoelectron microscopy, as well as optogenetic activation of FS cells to probe quantal amplitude at FS→SP synapses. Brief MD before p17 or p25 did not alter the density of FS→SP contacts. However, at the ultrastructural level, FS→SP synapses in deprived hemispheres during the CP, but not the pre-CP or in GAD65 knock-out mice, had larger synapses and increased docked vesicle density compared with synapses from the nondeprived control hemispheres. Moreover, FS→SP evoked miniature IPSCs increased in deprived hemispheres when MD was initiated during the CP, accompanied by an increase in the density of postsynaptic GABAA receptors at FS→SP synapses. These coordinated changes in FS→SP synaptic strength define an expression pathway modulating excitatory output during CP plasticity in visual cortex.