What is it about?
Altered signaling of type 1 metabotropic glutamate receptors is implicated in the pathophysiology of fragile X syndrome. The study shows altered functional responses to metabotropic glutamate receptor 5 (mGluR5) and identified altered differentiation of a subpopulation of mGluR5-responsive cells in mouse tissue-derived and human induced pluripotent stem cell-derived neural progenitors lacking fragile mental retardation protein.
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Why is it important?
The study shows that mGluR5 signaling contributes to the altered differentiation of neural progenitors in fragile X syndrome. The defects of mGluR5 signaling were shown to be similar in human and mouse progenitors but progenitor type-dependent differences were observed in responses to mGluR5 antagonist between mouse and human progenitors. The results validate the use of human iPS-derived neural progenitors in studies investigating the role of mGluR5 during early differentiation of neural progenitors in fragile X syndrome.
Perspectives
The studies identified subpopulations of glutamate-responsive cells during early differentiation of neural progenitors and provided evidence that alterations of these subpopulations may contribute to the abnormalities of neuronal circuit formation and function in fragile x syndrome.
Dr. Maija L Castrén
Helsingin Yliopisto
Read the Original
This page is a summary of: Metabotropic glutamate receptor 5 responses dictate differentiation of neural progenitors to NMDA-responsive cells in fragile X syndrome, Developmental Neurobiology, July 2016, Wiley,
DOI: 10.1002/dneu.22419.
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