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. 2017 Jun 12;8:271. doi: 10.3389/fneur.2017.00271

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Copyright © 2017 Kim, Yum, Lee, Kim, Shim and Ko.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Enhanced NMDA-induced spasm susceptibility and effects of anti-epileptic drugs in prenatally MAM-exposed infant rats treated with single (SD) or multiple (MD) N-methyl-d-aspartate (NMDA) doses. (A) MAM-exposed rats (MAM-SD, n = 15 at postnatal day (P) 12, n = 8 at P13, n = 10 at P15) showed significantly increased numbers of spasms in response to single NMDA doses at P12 (65.3 ± 6.2 vs. 35.1 ± 5.9, p = 0.003) and P13 (18.8 ± 3.8 vs. 4.4 ± 1.2, p = 0.002) compared to prenatally saline-exposed rats (control-SD, n = 9 at P12, n = 8 at P13, n = 6 at P15). (B) The latency to onset of spasms did not differ significantly between MAM and control groups treated with a single NMDA dose. (C) MAM-exposed rats exhibited significantly greater numbers of spasms in response to repeated NMDA administration on P12, P13, and P15 (MAM-MD, n = 15; 65.3 ± 6.2 at P12, p = 0.003; 80.1 ± 7.2 at P13, p = 0.001; 74.5 ± 10.1 at P15, p = 0.002) compared to prenatally saline-exposed rats (control-MD, n = 9, 35.1 ± 5.9 at P12, 31.7 ± 3.2 at P13, 29.6 ± 6.0 at P15). The number of spasms differed significantly between the control and the MAM groups over time (p < 0.001). (D) The latency to onset of spasms was significantly shorter in MAM rats than in controls with a significant group × time interaction (p = 0.032). The mean latency to onset of spasms in the MAM-MD group at P13 (1,313.7 ± 57.6 s) was significantly shorter than that in the control-MD group (1,543.8 ± 78.3 s, p = 0.03). (E) In MAM-SD rats, vigabatrin (VGB) significantly reduced the number of spasms at 125 mg/kg (VGB125, n = 11, 8.8 ± 2.6, p < 0.001) and 250 mg/kg (VGB250, n = 8, 4.3 ± 1.0, p < 0.001) compared to VGB-naïve MAM group rats (n = 10, 42.7 ± 6.4). (F) Pretreatment with VGB125 and VGB250 significantly prolonged the mean latency to onset of tailing (VGB125, 1,404.8 ± 70.5 s, p = 0.01; VGB250, 1,660.4 ± 113.8 s, p = 0.001) and first full spasms (VGB125, 2,047.8 ± 153.5 s, p = 0.012; VGB250, 2,246.9 ± 398.3 s, p = 0.016) compared to VGB-naïve MAM group rats (tailing, 1,091.5 ± 80.7 s; first full spasm, 1,480.9 ± 82.1 s) dose-dependently. In contrast, adrenocorticotropic hormone (ACTH, n = 6) had little effect on the number of spasms and the latency to onset of spasms. Values expressed as mean ± SEM. *p < 0.05 using Mann–Whitney U test for comparison between the two groups. ^†p < 0.05 using repeated measure ANOVA for main effect of group (between group) on the number of spasms or the latency to onset of spasms. ^‡p < 0.05 using repeated measure ANOVA for interaction effect of time-by-group on the number of spasms or the latency to onset of spasms.

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