Tinnitus is the most common disease in Otology, and extremely difficult for treatment in clinic, abnormal events in the cochlea (the abnormal events can result in abnormal neuronal activity in central auditory pathways that can then be finally perceived as tinnitus). Neuroplasticity events at the auditory cortex (AC) have been reported to include hyperactive of cortical neurons and an increase in neuronal synchronization. Our recent studies showed the changes markedly, in the expression of the excitatory glutamate receptor subtype NR2B in mRNA and protein levels, and also some changes in synaptic ultrastructure of neurons in auditory cortex of tinnitus animal. We propose that the mechanisms of tinnitus centralization may arise from abnormal events in the cochlea, and result in abnormal neuronal activity at multiple levels which promote abnormal propagation of neural activity in the central auditory pathway. The plastic change may be positive and adaptive as with learning or memory, or in the compensation after abnormal events in the cochlea that results in new neuronal networks that restore normal function. Alternatively, the neuroplasticity changes might be maladaptive leading perhaps to an imbalance in excitatory and inhibitory events in the brain. Indeed, tinnitus may be the consequence of such maladaptive neuroplasticity brain alterations (synaptic structure) has even gone a step further and described tinnitus as the perceptual manifestation of plastic brain changes that result in abnormal neuronal activity. The neuroplasticity changes may also make tinnitus persists, eventually leading to the existence of tinnitus cochlear-originated in the central pathway. They may also extend to non-sensory areas of the brain giving rise to the attentional and emotional aspects that often accompany the disorder. New pathophysiological insights maybe prompt the development of management approaches to directly target the neuroplasticity processes correlates of tinnitus.