Neuropeptide release is impaired in a mouse model of fragile x mental retardation syndrome

Suresh P. Annangudi, Agatha E. Luszpak, Soong Ho Kim, Shifang Ren, Nathan G. Hatcher, Ivan Jeanne Weiler, Keith T. Thornley, Brian M. Kile, R. Mark Wightman, William T. Greenough, Jonathan V. Sweedler

Research output: Contribution to journalArticlepeer-review


Fragile X syndrome (FXS), an inherited disorder characterized by mental retardation and autism-like behaviors, is caused by the failure to transcribe the gene for fragile X mental retardation protein (FMRP), a translational regulator and transporter of select mRNAs. FXS model mice (Fmr1 KO mice) exhibit impaired neuropeptide release. Release of biogenic amines does not differ between wild-type (WT) and Fmr1 KO mice. Rab3A, an mRNA cargo of FMRP involved in the recruitment of vesicles, is decreased by â50% in synaptoneurosomes of Fmr1 KO mice; however, the number of dense-core vesicles (DCVs) does not differ between WT and Fmr1 KO mice. Therefore, deficits associated with FXS may reflect this aberrant vesicle release, specifically involving docking and fusion of peptidergic DCVs, and may lead to defective maturation and maintenance of synaptic connections.

Original languageEnglish (US)
Pages (from-to)306-314
Number of pages9
JournalACS Chemical Neuroscience
Issue number4
StatePublished - Apr 21 2010

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Cognitive Neuroscience
  • Cell Biology


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