Activity Dependent Plasticity allows the central auditory system to adjust, react and adapt to changes in inputs.  When working properly, activity dependent plasticity provides enhanced processing and allows for “active listening”, a focus on salient input and suppression of other channels.  However, extremes of activity, such as deafness and noise can overwhelm the mechanisms of activity dependent plasticity and cause unwanted changes.  These changes lead to Tinnitus and Central Auditory Processing Disorders.

We therefore study the mechanisms of central auditory plasticity, the changes that occur following the extremes of deafness or noise and their correlation with Tinnitus and Central Auditory Processing Disorders.  We find that the changes resulting from either noise or deafness upset the delicate balance between excitation and inhibition.  This can lead to regions of increased excitability that may be associated with tinnitus, as well as regions of decreased excitability.  

Our studies focus on changes in excitatory synaptic strength (the excitatory transmitter glutamate and its receptors), changers in inhibitory synaptic strength (the inhibitory transmitters GABA and glycine and their receptors) as well as changes in the ion channels that regulation neuronal excitability, such as the 2-pore domain potassium channels.  Examples of results are shown below and also available in our recent manuscripts.

Photomicrograph comparing glycine immunostaining in the cochlear nucleus
of a normal hearing versus a 2 week deafened rat

Quantitative real-time PCR comparing glutamate receptor subunit expression
in the rat cochlear nucleus in normal hearing (dark bar) versus 3 weeks deafened
(light bar) animals

Figure showing decreased expression in the rat inferior colliculus of 2-pore domain potassium subunits at 3 days, 3 weeks and 3 months following deafness

Introduction

Our studies are based on the model of Lateral Olivocochlear Efferent function shown in the figure below, where different transmitters act to change the “set-point” of the auditory nerve.  This action provides increased sensitivity and increased dynamic range for the auditory nerve.  Our experiments use lesions with neurotoxins such as MPTP to study the mechanisms of function and to model disorders caused by dysfunction.

Auditory Anatomy:

• Richard Altschuler
• Yilei Cui
• Soo Duk Lee
• Cathy Lomax
• Ling Tong
• Noel Wys

KHRI Collaborators:

• Sanford Bledsoe
• David Dolan
• Margaret Lomax
• Josef Miller
• Susan Shore

Outside Collaborators

Wayne State University:

• Avril Genene Holt

University of Florida:

• Colleen LePrell Garbe

Kansai Medical University:

• Mikiya Asako
• Hiromichi Kuriyama

University of California, San Francisco:

• Russell Snyder

University of Connecticut:

• Douglas Oliver

Universidad de Castilla, LaMancha:

• Jose Juiz