Issue Cover (July 2018)

Front cover: Background: Long‐lasting forms of memory and synaptic plasticity such as late long‐term potentiation (L‐LTP) are dependent on protein synthesis. The aim of our study is to investigate potential interactions between signaling pathways controlling protein synthesis in hippocampal L‐LTP. Main findings: We found in mice that L‐LTP failure caused by inhibition of the mammalian target of rapamycin complex 1 (mTORC1) is prevented by genetic deletion of PERK, a kinase for eukaryotic initiation factor 2α (eIF2α). A key mechanism responsible for the L‐LTP rescue may involve down‐regulation of translational factor eEF2 phosphorylation, which is associated with increased protein synthesis capacity via its upregulation on mRNA translation elongation. Implication: These data, for the first time, connect reduction of PERK activity with the regulation of translation elongation in enabling L‐LTP independent of mTORC1. Image content: This image (63x) taken by confocal laser scanning microscope shows area CA1 of an acute hippocampal slice from wild‐type mouse that was labeled for phospho‐eEF2 (green) and DAPI (blue). Phospho‐eEF2 is distributed in both soma and dendrites.Read the full article ‘ Genetic removal of eIF2α kinase PERK in mice enables hippocampal L‐LTP independent of mTORC1 activity ’ by H. R. Zimmermann, W. Yang, B. C. Beckelman, N. P. Kasica, X. Zhou, L. D. Galli, A. G. Ryazanov, T. Ma ( J. Neurochem . 2018, vol. 146 (2), pp. 133–144) on doi: 10.1111/jnc.14306