|The mGluR Theory and Stress-Induced Plasticity in the Amygdala: Implications for Affective Symptoms in Fragile X
This project is being conducted in India, where the modest budget funds 1 postdoctoral fellow and 2 research assistants working full time on this project.
by Sumantra Chattarji, 2/1/2005
A growing body of evidence supports the “mGluR theory” which proposes that aspects of fragile X syndrome are a consequence of exaggerated metabotropic glutamate receptor (mGluR) function. This theory accounts for many symptoms of fragile X and integrates molecular and cellular correlates of the disease with basic research findings on synaptic plasticity mechanisms. Most studies to date have focused on the hippocampus, cerebellum, and cortex. However, emotional or mood-related symptoms of Fragile X, including anxiety and aggression, are likely to involve changes in the amygdala (the brain’s central emotion processor). No comprehensive studies have examined amygdalar plasticity in the context of the mGluR theory.
This project extends the mGluR theory into the domain of amygdalar plasticity. We are building on our findings on amygdalar function that relate to three key elements of the disease – (i) spine morphology, (ii) mGluR-mediated synaptic plasticity, and (iii) anxiety-like behavior.