Translating the MAM model of psychosis to humans. Issue 3 (March 2015)

• Record Type: Journal Article
• Authors: Modinos, Gemma; Allen, Paul; Grace, Anthony A.; McGuire, Philip
• Is Part Of: Trends in neurosciences. Volume 38:Issue 3(2015)
• Page Start: 129
• Page End: 138
• Publication Date: 2015-03
• Subjects: neurobiology -- psychosis -- neuroimaging -- animal research -- schizophrenia -- prodrome; Neurology -- Periodicals; Neurophysiology -- Periodicals; Neurobiology -- Periodicals; 612.8
• DOI: 10.1016/j.tins.2014.12.005
• Languages: English
• ISSNs: 0166-2236

Abstract

Highlights: Contemporary animal models of psychosis propose that: Elevated dopamine function is driven by altered MTL output. Alterations in the hippocampal–midbrain–striatal circuit have a critical role. Data from human studies are broadly consistent with predictions from animal models. Animal models are informing the development of new treatments of psychosis. Abstract : 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.