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. 2015 Mar 12;2(4):401–416. doi: 10.1002/acn3.183

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© 2015 The Authors. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Methyl supplementation reverses hippocampal memory deficits associated with epilepsy. (a) Diagram of experimental setup. (b) Methyl supplementation rescued memory impairments in the epileptic animals in the contextual fear conditioning (CFC) paradigm (F_3,36 = 5.95, P < 0.01, n = 10–11, one-way analysis of variance [ANOVA] with post hoc test, *significance relative to non-epileptic group). (c) Methyl supplementation rescued memory deficits in the epileptic animals in the object location (OL) paradigm (F_3,19 = 7.06, P < 0.01, n = 5–6, one-way ANOVA with post hoc test, *significance relative to non-epileptic group). (d) Methyl supplementation had no effect on fear conditioning training (F_3,26 = 7.68, P < 0.01, n = 7–9, one-way ANOVA with post hoc test, *significance relative to non-epileptic group; ^#significance between experimental groups). (e) Methyl supplementation with Met did not significantly alter movement time in the open-field paradigm. Epileptic animals showed greater mobility compared to non-epileptic rats (F_3,24 = 5.53, P < 0.01, n = 6–8, one-way ANOVA with post hoc test, *significance relative to non-epileptic group; ^#significance between experimental groups). (f) Methyl supplementation with Met did not alter the time spent in the open arena during the open-field paradigm (F_3,24 = 1.46, P > 0.05, n = 6–8, one-way ANOVA with post hoc test). Error bars are SEM.