AMPK has been shown to be integral to synaptic plasticity, learning, and memory, and the α subunit has proven essential for such processes. Its dysregulation has been implicated in diseases characterized by cognitive impairment such as Alzheimer disease; however, little is known about the neuronal effects of the β subunit. There exists evidence that AMPKβ has an auto-inhibitory effect on AMPK activity; thus, suppression of one or both AMPKβ isoforms (β1 and β2) could impact AMPK activity and cognitive function. Here, AMPKβ1 or β2 was conditionally knocked down in excitatory neurons of C57BL/6 mice (β1KD, β2KD) and behavioral tests were used to assess their learning and memory. Additionally, hippocampal de novo protein synthesis was assessed via the Surface Sensing of Translation (SUnSET) assay, and the phosphorylation of various AMPK-related signaling molecules was assessed via western blot. Furthermore, dendritic structure and function were assessed via synaptic electrophysiology, Golgi staining, and electron microscopy. Behavioral analysis showed an impairment in recognition memory of β2KD (not β1KD) mice but, interestingly, unaltered spatial memory in both groups. Electrophysiology revealed impairment of hippocampal long-term potentiation (LTP) in β2KD (not β1KD) mice. Further, dendritic spine maturity and postsynaptic density size & abundance were altered in β2KD mice. Moreover, AMPK activity (measured by phosphorylation of AMPKα’s Thr172 site) was decreased in the β2KD hippocampus, but unaltered in β1KD mice. Overall protein translation, as assessed by SUnSET, was unaltered. Together, these data suggest a previously unrecognized role for AMPKβ2 in regulation of postsynaptic morphology, hippocampal LTP, and recognition memory.