Panford-Walsh R1*, Rüttiger L1*, Singer W1*, Tan, J1, Kilian, S1, Schulze H2, Geisler H1, Köpschall I1, Rohbock K1, Zimmermann U1, Knipper M1
1University of Tübingen, Department of Otorhinolaryngology, Hearing Research Center Tübingen, Molecular Neurobiology, Elfriede-Aulhorn-Straße 5, D-72076 Tübingen, Germany
Leibniz Institute for Neurobiology, Brenneckestrasse 6, 39118 Magdeburg,
Germany
* equal contribution
Corresponding author:
tel. +49 (0)7071-29 88246
fax +49 (0)7071-294950
e-mail Marlies.Knipper@uni-tuebingen.de

Aberrant neuronal activity is known to lead to changes in neuronal plasticity. However, the molecular changes following sensory trauma and the subsequent response of the central nervous system are only poorly understood. We focused on finding a molecular tool for monitoring the features of excitability which occur following acoustic and ototoxic trauma to the auditory system. Of particular interest are genes that alter their expression pattern during activity-induced changes in synaptic efficacy and plasticity. The expression of brain-derived neurotrophic factor (BDNF) and the activity-dependent cytoskeletal protein (Arg3.1/arc) were monitored
in the peripheral and central auditory system hours and days following tinnitus- inducing traumatic stimuli or salicylate treatment. Tinnitus induction was monitored in a rodent animal behavior model. Excitatory input to the rat AI were investigated by local field potential (LFP) post pure-tone acoustic trauma using chronic implantion of 8 channel microelectrode arrays. BDNF and Arg3, were monitored at
the mRNA and protein level in the cochlea and subcortical and cortical areas. We present here a summary of recent findings comparing and correlating the expression of activity dependent genes with tinnitus-behavior. The data are discussed in the context of using the monitoring of activity-dependent genes to screen for the pharmacological reversal of tinnitus.

Supported by a grant from the Deutsche Forschungsgemeinschaft Kni-316/3-3.