Journal
TRENDS IN NEUROSCIENCES
Volume 38, Issue 3, Pages 129-138Publisher
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2014.12.005
Keywords
neurobiology; psychosis; neuroimaging; animal research; schizophrenia; prodrome
Categories
Funding
- Wellcome Trust [091667]
- NARSAD [21200]
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Elevated dopamine function and alterations in medial temporal lobe (MTL) structure and function are two of the most robust findings in schizophrenia, but how interactions between these abnormalities underlie the onset of psychosis is unclear. The methylazoxymethanol acetate (MAM) rodent model proposes that psychosis develops as a result of a perturbation of MTL function, leading to elevated striatal dopamine dysfunction. Here, we review several recent neuroimaging studies that examine components of the putative model in humans with an ultra high risk (UHR) of the psychosis. While data from these studies are broadly consistent with the MAM model, caution is required when comparing data across animal and human studies.
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