AAV-mediated Kcnmb2 overexpression in dorsal CA1 abolished these changes in neuronal excitability and synaptic transmission and improved LTP, as well as spatial learning and memory impairments in MD F1 mice [for behavioral results, see our previous study (Ryan et al., 2017)], supporting a model whereby repression of Kcnmb2 drives neural and cognitive alterations that occur in MD F1 offspring as a consequence of excessive paternal methyl donor intake. This evidence concerns the gene KCNMB2 and memory impairment.