Loss of glutamate transporter GLAST (EAAT1) causes locomotor hyperactivity and exaggerated responses to psychotomimetics: rescue by haloperidol and mGlu2/3 agonist

BACKGROUND: Recent data suggest that excessive glutamatergic signaling in the prefrontal cortex may contribute to the pathophysiology of schizophrenia, and that promoting presynaptic glutamate modulation via group II metabotropic glutamate (mGlu2/3) receptor activation can exert antipsychotic effica...

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Hlavní autoři: Karlsson, Rose-Marie, Heilig, Markus, Holmes, Andrew
Médium: Artigo
Jazyk:Inglês
Vydáno: 2008
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Article
On-line přístup:https://ncbi.nlm.nih.gov/pmc/articles/PMC2696047/
https://ncbi.nlm.nih.gov/pubmed/18550032
https://ncbi.nlm.nih.govhttp://dx.doi.org/10.1016/j.biopsych.2008.05.001
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