Changes in somatosensory evoked potentials in rats following transient cerebral ischemia

Background. Cerebral ischemia induced by transient middle cerebral artery occlusion is one of the most popular ischemic stroke models used to evaluate drug candidates with neuroprotective properties. The possibilities of combining this model with neurophysiological techniques (e.g., electroencephalography, electrocorticography, evoked potential registration, etc.) to assess the effectiveness of novel pharmacotherapeutic strategies appear to be of great interest to current biomedical research.

The aim. Identifying specific changes in somatosensory evoked potentials occurring after cerebral ischemia induced by middle cerebral artery occlusion in rats.

Materials and methods. A total number of 18 white outbred male rats were randomized into 3 groups by 6 animals in each: 1) control (presumably healthy animals); 2) ischemia-30 (30-minute middle cerebral artery occlusion); 3) ischemia-45 (45-minute occlusion). At post-surgery day 7, cortical responses to sequential electrical stimulation of left and right n. ischiadicus were registered. N1, P2, N2, P3, and N3 peak latencies and amplitudes, peak-to-peak interval durations and amplitudes were calculated. Spearman’s rank correlation coefficients were used to assess the relationship between ischemia duration and evoked potential parameters, and the Chaddock scale was used to qualitatively evaluate the strength of correlations.

Results. The rats subjected to cerebral ischemia demonstrated a decrease in some of the peak amplitudes of the ipsi- and contralateral somatosensory potentials evoked by n. ischiadicus stimulation. In the injured hemisphere, decreased P2 and N3 peak and P3–N3 interval amplitudes were registered ipsilaterally, and decreased P3 peak amplitudes and N2–P3 interval durations were observed contralaterally.

Conclusions. The obtained data suggest that somatosensory evoked potential registration and analysis can be used to evaluate the functional state of central nerve tracts in rats subjected to cerebral ischemia.

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