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Uncovering glutamatergic mechanisms behind motivational and cognitive deficits in drug addiction

 

Dysregulation of forebrain glutamatergic neurotransmission and plasticity is a common pathology in many neuropsychiatric disorders. Both studies in human addicts and preclinical drug addiction research revealed glutamatergic hypofunction during abstinence and glutamatergic hyperactivity during drug craving. While the hypoglutamatergic state has been linked to cognitive deficits (hypofrontality), excessive release of glutamate predicts high rates of relapse, and both phenomena complicate addiction treatment and recovery. Our lab has been studying metabotropic glutamate receptors (mGlu) in animal models of psychostimulant addiction to characterize immediate and prolonged changes in mGlu function and to test novel interventions at these receptors that could alleviate behavioral deficits associated with addiction. I will present our recent findings on the role of mGlu5 receptors in cocaine-seeking and post-cocaine cognitive deficits. Additionally, I will discuss whether dysregulation of mGlu5 receptor is a neurobiological marker of individual stress/addiction vulnerability.

 


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