Former studies of the same group provided evidence for improvement of learning in transgenic mice by overexpression of the NR2B subunit of the NMDA receptor. The present paper extends these findings to rats. Transgenic rats in which NR2B is overexpressed in the cortex and hippocampus show an enhanced LTP (but, contrary to expected prediction, not enhanced LTD) in CA1 and improved memory performance in several tasks (novel object recognition, water-maze, working memory in a T-maze). These important results provide evidence for the general role in animal species of the NR2B as “a universal genetic factor that acts as rate-limiting molecule in controlling memory function”. Of course, as mentioned by the authors, the precise role of NR2A has to be investigated in further work.