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. 2017 Sep 8;7:10995. doi: 10.1038/s41598-017-11316-8

Figure 3.

Figure 3

CN2097 attenuates TBI-induced hippocampal LTP deficits. Rats were injected i.p. with CN2097 (10 mg/kg) or vehicle (0.9% NaCl) at 1 and 2 h post-TBI. Extracellular field potentials (fEPSP) to Schaffer Collateral stimulation were recorded in CA1 at 1 and 3 days following treatment. (A) LTP was recorded in both the contralateral (Contra-Hip) and ipsilateral (Ipsi-Hip) hippocampal slices at 1 d (A1) and 3 d (A2) following vehicle (left) and CN2097 treatment (right). Left: Following TBI, LTP (2 × 100 Hz for 1 s, 20 s apart; arrows) was impaired in the ipsilateral (Ipsi-Hip, red), but not the contralateral hippocampus (Contra-Hip, black). Right: CN2097 restored LTP to control levels. Field EPSP slopes in the CA1 region are plotted as a percentage of baseline. Insets: Examples of fEPSP traces representing averages of 20 responses at baseline and LTP (Contra, black; Ipsi, red). (B) Group data of LTP in vehicle- and CN2097-injected rats at 1 d (B1) and 3 d (B2) following TBI. (B1) At 1 d after TBI and vehicle treatment, LTP was significantly impaired in the ipsilateral compared to contralateral hippocampus. After CN2097 treatment, LTP was restored in the ipsilateral hippocampus to a level that was not significantly different from that observed in the contralateral hippocampus. (B2) At 3 d following TBI, synaptic plasticity was similarly restored. In CN2097-treated rats, LTP in the ipsilateral hippocampus was not different from that observed in the contralateral hippocampus, while vehicle treatment resulted in a significant interhemisphere difference (C). Interhemisphere ratio (Ipsi/Contra) of LTP indicates highly impaired LTP in the ipsilateral hemisphere of vehicle-treated rats (yellow) when compared to CN2097-treated rats (blue) at 1 d as well as at 3 d post-TBI. Data represent mean ± SEM.