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Fragile X Mental Retardation Protein is Required for Chemically-induced Long-term Potentiation of the Hippocampus in Adult Mice

Fragile X syndrome (FXS) is caused by the lack of fragile X mental retardation protein (FMRP). The animal model of FXS, Fmr1 knockout (KO) mice, shows impairment in hippocampus-dependent learning and memory. However, results for long-term potentiation (LTP), remain inconclusive in the hippocampus of Fmr1 KO mice. Here, we demonstrate that FMRP is required for glycine-induced LTP (Gly-LTP) in the CA1 of hippocampus. The Gly-LTP requires activation of postsynaptic NMDA receptors and metabotropic glutamateric receptors, as well as the subsequent activation of extracellular signal-regulated kinase (ERK) 1/2. However, paired-pulse facilitation was not affected by glycine treatment. Our study provide evidences that FMRP participates in Gly-LTP by regulating the phosphorylation of ERK1/2, and that improper regulation of these signaling pathways may contribute to the learning and memory deficits observed in FXS.

Identiferoai:union.ndltd.org:TORONTO/oai:tspace.library.utoronto.ca:1807/18857
Date15 February 2010
CreatorsShang, Yuze
ContributorsZhuo, Min
Source SetsUniversity of Toronto
Languageen_ca
Detected LanguageEnglish
TypeThesis

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