Abstract
The molecular/cellular plasticity mechanisms that ensure adaptive animal behaviors remain less than fully understood. Our lab has shown that Rem2, a small GTPase of the Ras-like superfamily, regulates multiple plasticity-related phenomena, including synapse formation and function and dendritic arbor complexity. While the above work involved examination of visual cortex, Rem2 is also expressed the hippocampus, a region that mediates a broad swath of learning and memory behaviors, including Social Transmission of Food Preference (STFP) and the Morris Water Maze (MWM). For this thesis, I examined the hypothesis that Rem2 function is a vital part of hippocampal learning in mice, using these paradigms and other similar forms of learning that show evidence of being enhanced by hippocampal inactivation—specifically, conditioned taste aversion (CTA). In transgenic mice in which Rem2 was deleted specifically in hippocampus, STFP was ablated, and CTA was enhanced, a pattern of results that strongly suggests integral involvement in hippocampal learning-related processes. Surprisingly, a total Rem2 knockout had no effect on STFP (or MWM), suggesting that molecular mechanisms interact with distributed circuit function to control learning. By testing the role of Rem2 in behaviors that differentially recruit the hippocampus, we have added to our knowledge of molecules that underlie learning and memory in the hippocampus in addition to the role of the hippocampus in these learning and memory circuits.