synaptic plasticity and learning in animal models of tuberous sclerosis complex突触可塑性与学习在结节性硬化症动物模型复杂.pdfVIP

Hindawi Publishing Corporation Neural Plasticity Volume 2012, Article ID 279834, 8 pages doi:10.1155/2012/279834 Review Article Synaptic Plasticity and Learning in Animal Models of Tuberous Sclerosis Complex Timo Kirschstein Oscar Langendorff Institute of Physiology, University of Rostock, Gertrudenstrasse 9, 18057 Rostock, Germany Correspondence should be addressed to Timo Kirschstein, timo.kirschstein@uni-rostock.de Received 14 March 2012; Revised 11 May 2012; Accepted 16 May 2012 Academic Editor: Emma Frost Copyright © 2012 Timo Kirschstein. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Tuberous sclerosis complex (TSC) is caused by a mutation of either the Tsc1 or Tsc2 gene. As these genes work in concert to negatively regulate the mammalian target of rapamycin (mTOR) kinase which is involved in protein translation, mutations of these genes lead to a disinhibited mTOR activity. Both the clinical appearance of this condition including tumors, cognitive decline, and epileptic seizures and the molecular understanding of the mTOR signaling pathway, not only involved in cell growth, but also in neuronal functioning, have inspired numerous studies on learning behavior as well as on synaptic plasticity which is the key molecular mechanism of information storage in the brain. A couple of interesting animal models have been established, and the data obtained in these animals will be discussed. A special focus will be laid on differences among these models, which may be in part due to different background strains, but also may indicate pathophysiological variation in different mutations. 1. Introduction