Unilateral inner ear damage results in lasting changes in hippocampal CA1 field potentials in vitro.

We investigated the effects of a surgical lesion of one vestibular inner ear (unilateral vestibular damage [UVD]) on the field potential responses of CA1 neurons in vitro. Hippocampal slices were removed from rats at 4-6 weeks or 5-6 months post-UVD, and the field responses of CA1 neurons to electrical stimulation of the Schaffer collateral commissural pathway were analyzed. Compared with slices from sham and naive control animals, slices from UVD animals at 5-6 months post-UVD exhibited decreases in the population spike amplitude, the somal field excitatory postsynaptic potential (sfEPSP) slope, and the field EPSP (fEPSP) slope. For the population spike amplitude and fEPSP slope, this effect was observed in both CA1 ipsilateral and contralateral to the UVD. On both the ipsilateral and contralateral sides, paired-pulse testing showed increases in paired-pulse inhibition at the shortest interstimulus intervals (ISIs), with increases in paired-pulse facilitation at longer ISIs. This study provides the first evidence that peripheral vestibular damage can produce long-term changes in hippocampal electrophysiological activity in vitro.