Dopamine deficiency underlies learning deficits in neurofibromatosis-1 mice.
Children with neurofibromatosis type 1 (NF1) are prone to learning and behavioral abnormalities, including problems with spatial learning and attention. The molecular etiology for these deficits is unclear, as previous studies have implicated defective dopamine, cyclic adenosine monophosphate (cAMP)...
| Publicado en: | Annals of Neurology Vol. 73; no. 2; pp. 309 - 316 |
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| Autores principales: | , , , , , |
| Formato: | research Journal Article |
| Publicado: |
Wiley-Blackwell
Feb2013
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| Acceso en línea: | Ver este registro en EBSCOhost |
| fields | @attributes: recordID: 1 pdfLink: plink: https://search.ebscohost.com/login.aspx?direct=true&db=ccm&AN=104257174&site=ehost-live header: @attributes: shortDbName: ccm uiTerm: 104257174 longDbName: CINAHL Complete uiTag: AN controlInfo: bkinfo: dissinfo: jinfo: jid: 03645134 1WM jtl: Annals of Neurology issn: 03645134 maglogo: Y pubinfo: dt: Feb2013 vid: 73 iid: 2 pid: 480 pub: Wiley-Blackwell place: Malden, Massachusetts artinfo: ui: 104257174 NLM23225063 2012057399 10.1002/ana.23793 NLM23225063 PMC3608728 104257174 ppf: 309 ppct: 7 formats: tig: atl: Dopamine deficiency underlies learning deficits in neurofibromatosis-1 mice. aug: au: Diggs-Andrews, Kelly A Tokuda, Kazuhiro Izumi, Yukitoshi Zorumski, Charles F Wozniak, David F Gutmann, David H affil: Departments of Neurology, Washington University School of Medicine, St Louis, MO. sug: subj: Dopamine Learning Disorders Metabolism Learning Disorders Physiopathology Neurofibromatosis 1 Metabolism Neurofibromatosis 1 Physiopathology Animal Studies Attention Brain Stem Metabolism Brain Stem Physiopathology Hippocampus Metabolism Hippocampus Physiopathology Learning Disorders Etiology Memory Disorders Metabolism Memory Disorders Physiopathology Mice Neurofibromatosis 1 Complications Nucleotides Metabolism Proteins Signal Transduction Physiology ab: Children with neurofibromatosis type 1 (NF1) are prone to learning and behavioral abnormalities, including problems with spatial learning and attention. The molecular etiology for these deficits is unclear, as previous studies have implicated defective dopamine, cyclic adenosine monophosphate (cAMP), and Ras homeostasis. Using behavioral, electrophysiological, and primary culture, we now demonstrate that reduced dopamine signaling is responsible for cAMP-dependent defects in neuron function and learning. Collectively, these results establish defective dopaminergic function as a contributing factor underlying impaired spatial learning and memory in children and adults with NF1, and support the use of treatments that restore normal dopamine homeostasis for select individuals. pubtype: Academic Journal doctype: research Journal Article ougenre: Article language: English refInfo: holdings: @attributes: islocal: N |
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