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10.1016/j.tins.2014.12.005 http://scihub22266oqcxt.onion/10.1016/j.tins.2014.12.005 C4455929!4455929 !25554679     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25554679 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25554679 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Trends+Neurosci 2015 ; 38 (3 ): 129-38 Nephropedia Template TP {{tp|p=25554679 |t=2015. Translating the MAM model of psychosis to humans |pdf=|usr=}}{{25554679 }} gab.com Text Translating the MAM model of psychosis to humans JO: Trends Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25554679 #FOAvip 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. Twit Text FOAVip Translating the MAM model of psychosis to humans ????Trends Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25554679 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25554679 #FOAvip English Wikipedia <ref>{{Cite pmid|25554679 }}</ref> Translating the MAM model of psychosis to humans #MMPMID25554679 Modinos G ; Allen P ; Grace AA ; McGuire P Trends Neurosci 2015[Mar]; 38 (3 ): 129-38 PMID25554679 show ga 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. |Animals [MESH] |Brain/pathology/*physiopathology [MESH] |Disease Models, Animal [MESH] |Humans [MESH] |Methylazoxymethanol Acetate [MESH]Translating the MAM model of psychosis to humans (epmc).pdf DeepDyve Pubget Overpricing