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• W2140329216 abstract "Germline mutations in SPRED1 , a negative regulator of Ras, have been described in a neurofibromatosis type 1 (NF1)-like syndrome (NFLS) that included learning difficulties in some affected individuals. NFLS belongs to the group of phenotypically overlapping neuro-cardio-facial-cutaneous syndromes that are all caused by germ line mutations in genes of the Ras/mitogen-activated protein kinase extracellular signal-regulated kinase (ERK) pathway and that present with some degree of learning difficulties or mental retardation. We investigated hippocampus-dependent learning and memory as well as synaptic plasticity in Spred1 −/− mice, an animal model of this newly discovered human syndrome. Spred1 −/− mice show decreased learning and memory performance in the Morris water maze and visual-discrimination T-maze, but normal basic neuromotor and sensory abilities. Electrophysiological recordings on brain slices from these animals identified defects in short- and long-term synaptic hippocampal plasticity, including a disequilibrium between long-term potentiation (LTP) and long-term depression in CA1 region. Biochemical analysis, 4 h after LTP induction, demonstrated increased ERK-phosphorylation in Spred1 −/− slices compared with those of wild-type littermates. This indicates that deficits in hippocampus-dependent learning and synaptic plasticity induced by SPRED1 deficiency are related to hyperactivation of the Ras/ERK pathway." @default.
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• W2140329216 date "2008-12-31" @default.
• W2140329216 modified "2023-10-18" @default.
• W2140329216 title "<i>Spred1</i>Is Required for Synaptic Plasticity and Hippocampus-Dependent Learning" @default.
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• W2140329216 doi "https://doi.org/10.1523/jneurosci.4698-08.2008" @default.
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