Aims: 

Pathomechanism of schizophrenia is still unknown exactly. Possible causes include genetic mutations, neural injuries and increased stress, especially at young age. Symptoms of the disease can be divided into positive, negative and cognitive categories. Accordingly, patients with schizophrenia and corresponding animal model exhibit deficits in inhibitory control as measured using cognitive and electrophysiological paradigms. The aim of the present study was to develop a chronic animal model that reflects symptoms of disease including the changes in auditory evoked potentials (AEP).

Methods: 

Male Wistar rats (day 21 of age) were both housed individually for 4 weeks and treated with ketamine for 3 weeks. Three weeks after the re-socialization animals were implanted with cortical electrodes. Same intensity (70 dB) pair-click stimuli were applied 240 times. In a longitudinal study amplitudes and latencies of AEP waves were examined for several weeks. The ratio was calculated from amplitudes of responses to pair-click stimuli (test/condition ratio, T/C ratio).

Results: 

The amplitudes of the AEPs significantly decreased after the second click in both groups. The T/C ratio was higher (0.71±0.04 vs 0.54±0.02) and the latency of first wave was longer after both the first (19±0.8 vs 13±0.4 ms) and the second stimuli (17±1.3 vs 16±6.2 ms) in schizophrenic animals.

Conclusion: 

We can conclude that our chronic animal model showed prolonged dysfunctions of stimulus processing. These data suggest that this complex treatment can lead to an appropriate schizophrenia model at least in the respect of sensory gating.

Support: 

TÁMOP 4.2.2.-08/01-2008-0002 and OTKA (PD75156 and K68594) grants