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. 2010 Jul 21;30(29):9670–9682. doi: 10.1523/JNEUROSCI.1248-10.2010

Figure 8.

Figure 8.

Proposed model for how the experience-dependent structural remodeling of TC synapses maps onto physiological OD plasticity in mouse V1. A, Schematic of the primary visual pathway in mouse. B, Previous studies used chronic VEP recordings to monitor contralateral-eye (blue) and ipsilateral-eye (yellow) responses in V1 contralateral to the deprived eye (DE), which is dominated by contralateral input. Changes in responsiveness to binocular stimulation (B, dashed lines) are detected contralateral to the DE after 3 and 7 d of MC. Total TC synaptic drive in V1 is reduced by one-third after 3 d of MC and is caused by DE depression. After 7 d of MC, total TC synaptic drive is restored to pre-MC levels because of the subsequent potentiation of non-DE responses (yellow bars) [schematized VEP data adapted from Frenkel and Bear (2004)]. C, These changes are mirrored by the structural remodeling of net TC synaptic input detected in layer 4 (Figs. 5 A, 7 A). The diagram illustrates how MC-induced TC synaptic remodeling could occur in layer 4. Because the majority of neurons in mouse V1 are binocularly responsive and the relative magnitude of the input of each eye is reflected in the relative density of afferent input (Coleman et al., 2009), eye-specific input to a dendritic subregion of a binocular neuron is depicted by the relative number of TC synapses (ipsilateral TC input, yellow; contralateral TC input, blue). We propose that the depression of DE responses after 3 d of MC results from the weakening of layer 4 TC synapses, a subset of which is then targeted for elimination. Presynaptic terminals that provide driving input from DE axons (blue) have retracted by the time maximal depression has occurred. After 7 d of MC, two forms of presynaptic change that mirror physiological plasticity could account for deprivation-enabled potentiation: (1) The seemingly normal density of TC synapses could be explained by the addition of new synapses formed along TC axons serving the non-DE, and (2) the growth of existing non-DE synapses may also occur to restore the normal distribution of terminal size.