Acoustic over-exposure (AOE) triggers deafness in animals and in humans and provokes auditory nerve degeneration. One month after AOE, there is an increase in the cellular excitability within the dorsal cochlear nucleus (DCN) and this is considered as a possible neural correlate of tinnitus. The origin of this phenomenon is still unknown but it is suggested that it is triggered by plastic adjustments within the DCN arising at the early stages of deafness (Kaltenbach JA. 2007). The purpose of the present study was to determine how DCN excitability was affected 3-4 days after AOE. Wistar rats (14-16 days old) were anesthetized (0.15mg/kg fentanyl; 5.1 mg/kg fluanisone; 2.5 mg/kg midazolam _I.P)and exposed to a 110 dB SPL 15-kHz noise stimulus for 4 hours (AOE). In vivo auditory brainstem response recordings (anaesthesia as above) and in vitro whole-cell current-clamp recordings from brainstem slices containing the DCN were made 3-4 days post AOE. Auditory brainstem response recordings showed that the hearing thresholds were significantly elevated (between 20-30 dB SPL) for frequencies above 15 kHz. Control fusiform cells (the main output of the DCN) fired with a regular firing pattern as assessed by the coefficient of variation of the interspike interval distribution of 0.19 ± 0.11 (n=5). Three to four days after AOE, 30% of fusiform cells exhibited bursting irregular discharge patterns (coefficient of variation of the interspike interval distribution of 1.8 ± 0.6, n= 5; unpaired T test p<0.05). Control granule cells (interneurones projecting onto fusiform cells) fired with a high gain (slope of 2.5 ± 0.4 Hz/pA, n=10) that was decreased 3-4 days after AOE (to 1.4 ± 0.2 Hz/pA, n=9; unpaired T test p<0.05). This was accompanied by a decrease of their membrane resistance (from 1.9 ± 0.3 GΩ, n=10 to 1.1 ± 0.2 GΩ, n=10; unpaired T test p<0.05 ) and more hyperpolarized resting potentials (from -43 ± 4 mV, n=9 to -57 ± 4 mV, n=10; unpaired T test p< 0.05 ). Data obtained in fusiform cells and in granule cells recorded in control condition and after AOE were fitted with a leaky integrate-and-fire model. In conclusion we suggest that the DCN excitability changes occurring 3-4 days post AOE trigger the increased DCN excitability observed at a later stage and this represents the initial stages of tinnitus.