Cross-modal regulation of auditory cortex function

描述（由申请人提供）：最近的研究强调，每个初级感觉皮层不是孤立地工作，而是有一定程度的相互作用，这不仅对多感觉整合至关重要，而且对失去感觉模态时的感觉补偿也很重要。在盲人个体中，有几份报告称，交叉模态补偿允许增强剩余的感官。虽然跨模态可塑性在很大程度上有利于盲人个体，但它阻碍了临床干预的功能恢复。为

DESCRIPTION (provided by applicant): 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.