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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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| Autori principali: | , , |
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| Natura: | Artigo |
| Lingua: | Inglês |
| Pubblicazione: |
2008
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| Soggetti: | |
| Accesso online: | 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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