Abstract:
:Fragile X syndrome is a leading heritable cause of mental retardation that results from the loss of FMR1 gene function. A Drosophila model for Fragile X syndrome, based on the loss of dfmr1 activity, exhibits phenotypes that bear similarity to Fragile X-related symptoms. Herein, we demonstrate that treatment with metabotropic glutamate receptor (mGluR) antagonists or lithium can rescue courtship and mushroom body defects observed in these flies. Furthermore, we demonstrate that dfmr1 mutants display cognitive deficits in experience-dependent modification of courtship behavior, and treatment with mGluR antagonists or lithium restores these memory defects. These findings implicate enhanced mGluR signaling as the underlying cause of the cognitive, as well as some of the behavioral and neuronal, phenotypes observed in the Drosophila Fragile X model. They also raise the possibility that compounds having similar effects on metabotropic glutamate receptors may ameliorate cognitive and behavioral defects observed in Fragile X patients.
journal_name
Neuronjournal_title
Neuronauthors
McBride SM,Choi CH,Wang Y,Liebelt D,Braunstein E,Ferreiro D,Sehgal A,Siwicki KK,Dockendorff TC,Nguyen HT,McDonald TV,Jongens TAdoi
10.1016/j.neuron.2005.01.038subject
Has Abstractpub_date
2005-03-03 00:00:00pages
753-64issue
5eissn
0896-6273issn
1097-4199pii
S0896-6273(05)00076-0journal_volume
45pub_type
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