Abstract
The deletion of matrix metalloproteinase MMP9 is combined here with chronic monocular deprivation (cMD) to identify the contributions of this proteinase to plasticity in the visual system. Calcium imaging of supragranular neurons of the binocular region of primary visual cortex (V1b) of wild-type mice revealed that cMD initiated at eye opening significantly decreased the strength of deprived-eye visual responses to all stimulus contrasts and spatial frequencies. cMD did not change the selectivity of V1b neurons for the spatial frequency, but orientation selectivity was higher in low spatial frequency-tuned neurons, and orientation and direction selectivity were lower in high spatial frequency-tuned neurons. Constitutive deletion of MMP9 did not impact the stimulus selectivity of V1b neurons, including ocular preference and tuning for spatial frequency, orientation, and direction. However, MMP9−/− mice were completely insensitive to plasticity engaged by cMD, such that the strength of the visual responses evoked by deprived-eye stimulation was maintained across all stimulus contrasts, orientations, directions, and spatial frequencies. Other forms of experience-dependent plasticity, including stimulus selective response potentiation, were normal in MMP9−/− mice. Thus, MMP9 activity is dispensable for many forms of activity-dependent plasticity in the mouse visual system, but is obligatory for the plasticity engaged by cMD.
Highlights
The shift in ocular preference in binocular neurons of the primary visual cortex is the canonical model of receptive field plasticity confined to a postnatal critical period
MMP9 is obligatory for the plasticity engaged by chronic MD (cMD) at eye-opening, but is dispensable for many other forms of plasticity that refine and maintain the mouse visual system
This suggests that MMP9 is obligatory for the plasticity engaged by cMD from eye opening, but it is dispensable for other forms of plasticity that refine and maintain the mouse visual system
Summary
The shift in ocular preference in binocular neurons of the primary visual cortex is the canonical model of receptive field plasticity confined to a postnatal critical period. The critical period for ocular dominance plasticity peaks during the third postnatal week, after one week of binocular vision. MD during the critical period decreases the strength of deprived eye responses and the density of spines on the apical dendrites of supragranular neurons [2–4]. We have previously shown that the visual deficits induced by cMD can be reversed in adults by dark exposure followed by light reintroduction [11]. The pharmacological induction of synaptic potentiation increases MMP9 activity, at enlarging or emerging spines [24]. The reactivation of structural and functional plasticity in adult mouse V1 by light reintroduction following dark exposure requires an increase in activity of endogenous MMP9 [18]. The changes in neuronal response strength and selectivity induced by cMD in wild-type (WT) mice are absent in MMP9−/− mice
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