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Brain Development and Disorders Project

Colloquium Series


“The mGluR theory of fragile X mental retardation syndrome”

 

Mark F. Bear, Ph.D.

Picower Professor of Neuroscience

Picower Institute for Learning and Memory

Massachusetts Institute of Technology

Investigator, Howard Hughes Medical Institute



6:00 pm, Wednesday, May 17, 2006
MIT Building 46-3002 (auditorium), followed by a reception

Building Address: 43 Vassar Street, Cambridge, MA 02139

 

Please RSVP to lmavros@mit.edu

 

Many of the diverse functional consequences of activating group 1 metabotropic glutamate receptors require translation of pre-existing mRNA near synapses. One of these consequences is long-term depression (LTD) of transmission at hippocampal synapses. Loss of fragile X mental retardation protein (FMRP), the defect responsible for fragile X syndrome in humans, increases LTD in mouse hippocampus. This finding is consistent with the growing evidence that FMRP normally functions as a repressor of translation of specific mRNAs. A theory has been developed that can account for diverse neurological and psychiatric aspects of fragile X syndrome, based on the assumption that many of the protein-synthesis-dependent functions of metabotropic receptors are exaggerated in fragile X syndrome. The theory suggests new direction for basic research as well as novel therapeutic approaches for the treatment of humans with fragile X, the most frequent inherited cause of mental retardation and an identified cause of autism.

 

Supported by the Simons Foundation and the Anne and Paul Marcus Family Foundation