Recent studies highlight that each primary sensory cortex does not work in isolation, but have some degree of interaction, which is not only critical for multisensory integration, but also important for sensory compensation in the event of losing a sensory modality. In blind individuals, there are several reports of cross- modal compensation that allow enhancement of the remaining senses. While cross-modal plasticity is largely beneficial to blind individuals, it hinders the recovery of function by clinical interventions. For example, the success of recovering speech recognition following cochlear implants is reported to inversely correlate with the extent of cross-modal plasticity. It is likely that similar obstacls will be met when trying to restore vision in blind. While there are many studies on cross-modal plasticity, most analyses are done at the level of systems neuroscience. Therefore, there is scarce information as to what types of changes happen at the cellular and circuit level. We previously showed that depriving rodents of vision increases the excitatory synaptic transmission in primary visual cortex (V1), in line with homeostatic adaptation. Importantly, we also found that visual deprivation reduces the excitatory synaptic transmission in the superficial layers of primary auditory cortex (A1). These results suggest that losing vision can cross-modally alter synaptic function in other primary sensory cortices, but how these cellular level changes alter the neuronal and circuit function of A1 is unknown. In the current proposal, we will test our hypothesis that visual deprivation-induced synaptic plasticity alters the functional circuitry and the neuronal receptive field properties in A1. To do this, we will determine whether visual deprivation alters the synaptic strength (Aim 1-1) and spatial extent (Aim 1-2) of specific excitatory and inhibitory circuitry of A1. To examine the in vivo consequences, we will examine whether visual deprivation alters the receptive field properties of neurons (Aim 2-1) and the population encoding in A1 (Aim 2-2). Results from our study will provide a comprehensive mechanistic understanding of how visual deprivation changes the functionality of A1. Functional connectivity across different brain regions is not restricted to sensory cortices. Therefore, our findings can be generalized to elucidate how neurons globally adjust to insults to other parts of the brain, such as would occur during neural injury, stroke and neurodegeneration.
It is well documented that losing vision enhances the functionality of the remaining senses, such as hearing. This proposal aims to determine the changes in the circuits of the brain area involved in hearing (i.e. auditory cortex) following visin loss and link those changes to the sound processing properties of this area. The results from our study will shed light on how the brain adapts to losing vision, and will provide means to enhance or reverse these changes.
|Meng, Xiangying; Kao, Joseph P Y; Lee, Hey-Kyoung et al. (2017) Intracortical Circuits in Thalamorecipient Layers of Auditory Cortex Refine after Visual Deprivation. eNeuro 4:|
|Meng, Xiangying; Winkowski, Daniel E; Kao, Joseph P Y et al. (2017) Sublaminar Subdivision of Mouse Auditory Cortex Layer 2/3 Based on Functional Translaminar Connections. J Neurosci 37:10200-10214|
|Petrus, Emily; Rodriguez, Gabriela; Patterson, Ryan et al. (2015) Vision loss shifts the balance of feedforward and intracortical circuits in opposite directions in mouse primary auditory and visual cortices. J Neurosci 35:8790-801|
|Meng, Xiangying; Kao, Joseph P Y; Lee, Hey-Kyoung et al. (2015) Visual Deprivation Causes Refinement of Intracortical Circuits in the Auditory Cortex. Cell Rep 12:955-64|
|Lee, Hey-Kyoung; Whitt, Jessica L (2015) Cross-modal synaptic plasticity in adult primary sensory cortices. Curr Opin Neurobiol 35:119-26|
|Petrus, Emily; Isaiah, Amal; Jones, Adam P et al. (2014) Crossmodal induction of thalamocortical potentiation leads to enhanced information processing in the auditory cortex. Neuron 81:664-73|