Deafness Resarch Foundation (7/1/2006-6/30/2008)
Synaptic Organization and Plasticity in the Auditory Cortex Following Cochlear Ablation: Role of Serotonin

PI: Gregory Basura, M.D., Ph.D.

Hearing loss has become an identified growing problem.  Hearing loss during early development may cause deficiencies in speech development, sound discrimination, and cognitive function.  Clinically, this may lead to permanent loss of auditory perceptual skills and impaired language acquisition.  To date, hearing loss research has largely focused on cochlear and cochlear nuclei functioning in animal models of deafness, while alterations in the primary auditory cortex (A1) remain largely unexplored.  The present application will utilize intact developing postnatal rats as well as a rodent model of sensorineural hearing loss (SNHL) in order to understand the anatomical and physiological changes in the A1 that occur across normal developmental and after developmental  periods of bilateral hearing loss.  Specifically, this proposed project will evaluate changes in neuronal physiology across normal developmental and following early postnatal cochlear ablation.  Moreover, we also seek to understand how normal modulators of cerebral cortical development, like serotonin (5-HT) and 5-HT 2A receptors, may contribute to normal A1 development and to changes in A1 neurons after SNHL to better understand how plasticity in the A1 may compensate for hearing loss.  These studies seek to identify novel mechanisms leading to A1 regulation following hearing loss.