Molecular Neurobiology

, Volume 46, Issue 3, pp 662–681

The mTOR Signaling Pathway in the Brain: Focus on Epilepsy and Epileptogenesis

Authors

  • Emilio Russo
    • Science of Health Department, School of MedicineUniversity “Magna Graecia” of Catanzaro
  • Rita Citraro
    • Science of Health Department, School of MedicineUniversity “Magna Graecia” of Catanzaro
  • Andrew Constanti
    • Department of PharmacologyUCL School of Pharmacy
    • Science of Health Department, School of MedicineUniversity “Magna Graecia” of Catanzaro
Article

DOI: 10.1007/s12035-012-8314-5

Cite this article as:
Russo, E., Citraro, R., Constanti, A. et al. Mol Neurobiol (2012) 46: 662. doi:10.1007/s12035-012-8314-5

Abstract

Recent evidence suggests that an altered mammalian (mechanistic) target of rapamycin (mTOR) signaling pathway and its pharmacological modulation might be implicated in several neurological diseases including epileptogenesis. mTOR is a molecular sensor, which regulates protein synthesis, enhancing mRNA translation of genes involved in the regulation of cell proliferation and survival, working as part of two distinct multimeric complexes known as mTORC1 and mTORC2. mTOR is an evolutionarily highly conserved serine/threonine kinase belonging to the phosphoinositide 3-kinase-related kinase family and represents one of the most recently studied pathways in relation to epilepsy and epileptogenesis, due to its suggested pivotal role in many aspects of cellular proliferation and growth also including neurodegeneration, neurogenesis, and synaptic plasticity. In this review, we report the cellular and molecular features of mTOR and related pathways, analyze their function in the brain including all current related evidence of their role, and finally, discuss the possible involvement of mTOR signaling in epileptogenesis and epilepsy, giving further consideration to future developments in this area.

Keywords

RapamycinAntiepileptogenicTuberous sclerosis complex (TSC)SeizureTemporal lobe epilepsy (TLE)Inflammation

Copyright information

© Springer Science+Business Media, LLC 2012