It is well established that experience-dependent cortical plasticity is most prominent early in life, especially in the primary sensory cortices. However, distinct circuit components in the adult cortex retain their ability to undergo plasticity. For example, synapses in the superficial layers of primary sensory cortices remain plastic in adults, which contrasts thalamocortical inputs with limited plasticity. Determining the mechanisms of innate plasticity present in the adult sensory cortices will allow us to understand how the adult brain adapts to changes in sensory experience. We recently found evidence that in adult primary visual cortex (V1) select excitatory synapses undergo plastic changes with rather brief alterations in sensory experience. First, we found that brief alterations in visual experience preferentially changes the strength of lateral intracortical synapses to layer 2/3 (L2/3) neurons without changes in the strength of feedforward inputs from layer 4 (L4). Second, we found that deafening adults produces potentiation of thalamocortical synapses onto L4 neurons in V1 within a week. These findings suggest that adult V1 has rather rapid innate plasticity in response to changes in sensory experience. In this proposal, we aim to understand how specific inputs to L2/3 of adult V1 adapt to losing vision (Aim 1), and the mechanisms underlying their subsequent recovery (Aim 2). In addition, we will determine the mechanisms of thalamocortical synaptic plasticity elicited in adult V1 following a brief duration of deafening, and whether it can enhance ocular dominance plasticity (ODP) (Aim 3). The results from our work will shed light on how V1 adapts to changes in sensory experience later in life. Furthermore, our results will provide mechanistic understanding of adult V1 plasticity, and generate molecular tools to enhance or prevent such changes in a circuit specific manner. These developments will ultimately allow us to manipulate innate plasticity mechanisms present in adult V1 to promote functional recovery of vision.
Adult brain is less malleable than young, but specific circuit components in the adult brain retain the ability to adapt to changes in sensory experience. Investigating the plasticity mechanisms present in the adult brain will not only allow us to understand how it adapts to losing a sensory modality, but will also offer us tools to enhance or prevent plasticity for recovering normal function as adults. Furthermore, our results can be generalized to offer insights into how the adult brain adapts to neuronal insults, such as stroke, trauma or neurodegeneration.
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