mTOR Signaling: At the Crossroads of Plasticity, Memory, and Disease

By C. Hoeffer, E. Klann. Trends in Neurosciences, 2009

1,092 citations recorded by the source corpus.

Mammalian target of rapamycin (mTOR) is a protein kinase involved in translation control and long-lasting synaptic plasticity. mTOR functions as the central component of two multi-protein signaling complexes, mTORC1 and mTORC2, which can be distinguished from each other based on their unique compositions and substrates. Although majority of evidence linking mTOR function to synaptic plasticity comes from studies utilizing rapamycin, studies in genetically-modified mice also suggest that mTOR couples receptors to the translation machinery for establishing long-lasting synaptic changes that are the basis for higher order brain function, including long-term memory. Finally, perturbation of the mTOR signaling cascade appears to be a common pathophysiological feature of human neurological disorders, including mental retardation syndromes and autism spectrum disorders.

Subfields: Cellular and Molecular Neuroscience, Genetics, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/f59fea0caf230e7d4580f673adb42acc4bd93a8e

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Citations in the corpus

Cognitive dysfunction in psychiatric disorders: characteristics, causes and the quest for improved therapy (2012, background): “Similarly, cognitive deficits associated with the ASD-related disorder tuberous sclerosis are provoked by mutations in the genes encoding tuberous sclerosis protein 1 and tuberous sclerosis protein 2, which interact with mTOR (Supplementary information S2 (figure)); cognitive impairment may theref”
Loss of mTOR-dependent macroautophagy causes autistic-like synaptic pruning deficits (2014, neutral): “…convergent mechanism in ASD. mTOR signaling, however, contributes to protein synthesis required for neuronal survival, development, synaptic plasticity, learning, and memory (Hoeffer and Klann, 2010), and prolonged use of mTOR inhibitors may cause adverse effects (Rodrik-Outmezguine et al., 2011).”
Glutamate NMDA receptor antagonists rapidly reverse behavioral and synaptic deficits caused by chronic stress exposure (2011, positive): “The mTOR pathway has been implicated in activity-dependent synaptic plasticity and is localized in neuronal dendrites and spines where it controls the synthesis of proteins that are required for new synapse formation (26).”
Psychedelics Promote Structural and Functional Neural Plasticity (2018, background): “, 2005), the production of proteins necessary for synaptogenesis (Hoeffer and Klann, 2010), and the effects of ketamine (Dwyer and Duman, 2013; Li et al.”