Translating the MAM model of psychosis to humans

Gemma Modinos; Paul Allen; Anthony A. Grace; Philip McGuire

doi:10.1016/j.tins.2014.12.005

Translating the MAM model of psychosis to humans

Gemma Modinos, Paul Allen, Anthony A. Grace, Philip McGuire

Research output: Contribution to journal › Article

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.

Original language	English
Pages (from-to)	129-138
Journal	TRENDS IN NEUROSCIENCES
Volume	38
Issue number	3
DOIs	https://doi.org/10.1016/j.tins.2014.12.005
Publication status	Published - 2015

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10.1016/j.tins.2014.12.005

http://dx.doi.org/10.1016/j.tins.2014.12.005

Cite this

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title = "Translating the MAM model of psychosis to humans",

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.",

author = "Gemma Modinos and Paul Allen and Grace, {Anthony A.} and Philip McGuire",

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AU - Allen, Paul

AU - Grace, Anthony A.

AU - McGuire, Philip

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AB - 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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DO - 10.1016/j.tins.2014.12.005

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