mTOR Involvement in the Mechanisms of memory: An Overview of Animal Studies

Structural and functional modifications at synapses, which are dependent upon de novo protein synthesis, are required to stabilize long-term memories (LTM). In the adult brain, mammalian target of rapamycin (mTOR) modulates translation in specific cellular departments, including dendritic spines, directly regulating peripheral protein synthesis, independently from the nuclear transcription machinery. mTOR activation, enhancing protein translation in the somatodendritic compartment of neurons, is involved in synaptic plasticity and in the development of novel LTM, as demonstrated in different animal models in vivo and in vitro. While mTOR inhibition by rapamycin leads to memory deficits in several behavioral tasks, there are conditions in which dysregulation/ hyperactivation of mTOR can also lead to memory impairments. Indeed, the exact mechanism(s) downstream of mTOR activation involved in synaptic plasticity and memory have not been completely unraveled. In this chapter, the current view on the molecular mechanisms of mTOR in synaptic plasticity and memory is reported.