Each year over 15 million babies are born preterm (before 37 weeks of gestation). These children tend to exhibit long term visual and auditory impairments that are both peripheral and central in nature. This has been highly correlated with the sensory over-exposure that occurs in the NICU. These specialized medical facilities expose the infant to light and sound levels that are maladaptive to their developing sensory systems. Our model of NICU exposure uses highly controlled sensory stimulation to simulate the NICU in young animals. This is followed by long term study of the changes to peripheral and central sensory processing as a function of learning and memory impairments that emerge throughout life. Parallel experiments are designed to test pharmacological treatments and engineered forms of harmful sensory stimulus mitigation.

In children, both congenital (genetic) and progressive forms of hearing loss occur early in life. Often these can emerge as unilateral or bilateral forms of mild, moderate, and severe hearing loss at a time when the child is rapidly gaining information about the environment. If not treated properly (e.g., hearing aids/cochlear implants/sign language) this deprivation can lead to impairments in language acquisition and higher-order cognition. Our models use both reversible (earplugging) and permanent (malleus removal) forms of conductive and sensorineural (noise exposure) hearing loss to investigate how the auditory system responds to acute and permanent sensory deprivations during development. We then test these animals on various cognitive and perceptual behavioral paradigms as adults to study hearing loss induced learning impairments. These are coupled with neurophysiological measurements designed to discover how early hearing loss affects learning related plasticity and neuronal network function in juveniles and adults. We will use these insights to develop treatment strategies to improve learning and lessen the severity of cognitive impairments.

As you age, hearing loss inevitably occurs for everyone as the specialized cells in our inner ear called “hair cells” die. These progressive changes alter the way that sounds are processed by the brain, until a critical threshold occurs where behaviors such as listening in a crowd become difficult. Recently, this level of hearing loss has been connected to the onset of cognitive decline (e.g., dementia and Alzheimer’s disease). Because everyone will eventually fall victim to hearing loss, it is vital to understand how low levels of hearing loss accrue towards debilitating levels that emerge subsequent to the onset of aging cognitive disorders (dementia). Our models have been designed to study progressive hearing loss in adults by using noise exposure to quickly induce hearing loss. Here we will systematically investigate the relationship between hearing loss and cognitive impairment by using an extensive battery of cognitive behavioral paradigms coupled with neurophysiological techniques. It is our hope to find both pharmacological and “gene-therapy” based treatments that will prevent/reduce both the progressive hearing loss seen in aging individuals and the accompanying cognitive decline seen in the human population.

Third mobile window syndrome in humas is a disorder in which a hole in the bony labyrinth of the inner ear (cochlea/vestibule) leads to inadvertent sound induced activation of the vestibular system. The symptoms can be quite severe, with noise induced vertigo and confusion that can substantially lower the quality of life for these individuals. Surgical treatments involve plugging the boney dehiscence and lead to resolution of the symptoms for many; however, perseverative symptoms can occur in certain individuals (e.g., congenital TMWS). This includes lasting peripheral (balance/vertigo) and central (cognitive) impairments. Our model uses a semicircular canal dehiscence (the most common form of TMWS) to study the peripheral and central effects of acute and chronic vestibular dysfunction. We will use this model to track down the central mechanism that drive the maladaptive plasticity responsible for the lingering symptoms experienced by some individuals. Wit this information we will be able to begin developing treatments for those individuals who are not responsive to surgical treatment (pluggin).