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The majority of tinnitus cases are related to cochlear dysfunction, leading to altered peripheral input to the central auditory system [1]. These alterations are believed to increase the basic level of neural activity during off-conditions of sound and to diminish the increase in neural activity when sound is presented [2]. As a compensatory means the affected region of primary auditory cortex tries to maximize the difference between basic level activity and sound-induced activity by adapting inhibitory and excitatory influences towards less GABAergic inhibition. This adaptation in turn triggers unmasking of dormant synapses and creation of new connections through axonal sprouting and finally results in a reorganization of tonotopic receptive fields and the manifestation of tinnitus [3]. To further investigate the processes involved in tinnitus manifestation we used neuroConstruct [4] to implement a simulation of the primary auditory cortex. It consists of two groups of different types of neurons, excitatory regular spiking pyramidal cells and inhibitory fast spiking basket cells with a group size of ? and ?, respectively. Its organization is based on experimental data from animal studies. Neurons were modeled as conductance-based multi-compartment neurons having numerous ionic conductances to achieve the desired firing properties. Model neurons posses glutamate- (AMPA and NMDA) and GABA-sensitive synaptic receptors. Afferent input from the auditory pathway was modeled as trains of spikes. Their frequency depended on the strength of the input whereas their target site depended on the frequency of the input. Additionally, synaptic background noise was introduced to the system as Gaussian noise. Excitatory cells made connections to other

Early signs of tinnitus in a simulation of the mammalian primary auditory cortex