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Commentary
Cellscience Reviews Vol 5 No 1
ISSN 1742-8130 |
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Dopamine-glutamate interactions at the forefront of schizophrenia research
Yvette Fisher, Véronique M. André, Carlos Cepeda & Michael S. Levine
Mental Retardation Research Center, Semel Institute for Neuroscience and Human Behavior, University of California Los Angeles, CA 90095, USA.
Received 21st July © Cellscience 2008
Which animal model better reproduces the cognitive and behavioral abnormalities characteristic of schizophrenia? Although many models exist, few take into account the complexity and diversity of neurotransmitter interactions that are involved in this psychiatric disorder, in particular dopamine and glutamate receptor interactions. In a recent paper Wiedholtz et al. [33] report a mouse model in which deletion of the GluR1 subunit of the glutamate AMPA receptor results in schizophrenia-like behaviors, hyperdopaminergia and responds to typical antipsychotic agents. This model could represent an important tool for understanding schizophrenia and developing new therapeutic interventions.
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