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J Nucl Med. 2008; 49 (Supplement 1):130P
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Neurosciences: Basic Science

Emerging Ligands and Targets

Modulation of dopamine D2 and metabotropic glutamate type 5 receptors in a rat model of schizophrenia

Anna-Liisa Brownell1, Janelle Drouin-Ouellet2, Ji-Quan Wang1, Darshini Kuruppu1 and Francesca Cicchetti2

1 Radiology, Massachusetts General Hospital, Boston, Massachusetts; 2 Unite de Neuroscience, Laval University, Quebec, Quebec, Canada

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Objectives: We aim to test the hypothesis that abnormal neurotransporter function occurs in schizophrenia, and more specifically that dopamine D2 and metabotropic glutamate type 5 receptors (mGluR5) modulation is altered in an ibotenic acid induced rat model of schizopheria.

Methods: On post-natal day 7 (p7), 4 Sprague Dawley male pups underwent bilateral ibotenic acid (IA) lesions into the ventral hippocampus to generate permanent brain damage and post-pubertal behavioral deficits reminiscent of schizophrenia. Similarly, 4 pups were injected with saline to serve as controls. At adulthood (p50), PET imaging studies were conducted to investigate dopamine D2 receptors with [18F]fallypride and mGluR5 function with [18F]FPEB (3-[18F]fluoro-5-(2-pyridinylethynyl)benzonitrile).

Results: In IA-lesioned animals, we found enhanced [18F]fallypride binding in striatum (16±6%), hypothalamus (18±4%) and S1-S2 cortices (11±3%) compared to control animals indicating elevated dopamine D2 receptor function. The binding in the thalamus was decreased by (10±4%) while [18F]FPEB binding had the highest enhancement (25±6%) in the that area. Increased [18F]FPEB binding was also observed in the striatum (11±3%), S1-S2 cortices (17±6%) and hippocampus (6±3%) indicating elevated glutamatergic function.

Conclusions: The enhanced binding of [18F]fallypride and [18F]FPEB in IA-lesioned animals indicate enhanced dopamine D2 and mGluR5 function as well as modulation of the prominent transporters, dopamine and glutamate. Ongoing studies will shed light of the precise functional changes occurring in schizophrenia and more specifically, the implication of these changes to the development of the schizophrenic phenotype.

Research Support: NIBIB-R01EB001850





This Article
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Right arrow Email this article to a friend
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Right arrow Alert me to new issues of the journal
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Google Scholar
Right arrow Articles by Brownell, A.-L.
Right arrow Articles by Cicchetti, F.
PubMed
Right arrow Articles by Brownell, A.-L.
Right arrow Articles by Cicchetti, F.