Well, the NR2B gene is encoding for a very common and well known receptor within both rat and human brains - the NMDA receptor. These receptors have been the target of the majority of recent studies into working memory and synaptic plasticity, or so-called "long-term potentiation". Basically, the NMDA receptor is the most likely cause of memory reinforcement.
The idea is that when two neurons fire simultaneously, the connection between them is strengthened for a long period of time. That is, the post-synaptic neuron becomes more sensitive to input from the pre-synaptic neuron. This effect is input-specific, in that it is only effective between the two specific neurons involved, and no similar input from other pre-synaptic neurons is necessarily potentiated. Most LTP relies on the NMDA receptors to function, via the calcium ion channels within most synapses. This is why increasing the number of NMDA receptors would likely reflect a quantitative increase in memory.
This isn't exactly breaking news - researchers have known about the NMDA receptors/NR2B gene for years, and I've seen studies from several years ago with the same approximate findings in animal models.