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.

Public Health Relevance

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.

Agency
National Institute of Health (NIH)
Institute
National Eye Institute (NEI)
Type
Research Project (R01)
Project #
3R01EY022720-02S1
Application #
8871860
Study Section
Special Emphasis Panel (ZRG1-IFCN-B (03))
Program Officer
Steinmetz, Michael A
Project Start
2013-03-01
Project End
2018-02-28
Budget Start
2014-03-01
Budget End
2015-02-28
Support Year
2
Fiscal Year
2014
Total Cost
$67,495
Indirect Cost
$22,341
Name
Johns Hopkins University
Department
Neurosciences
Type
Schools of Arts and Sciences
DUNS #
001910777
City
Baltimore
State
MD
Country
United States
Zip Code
21218