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Carlisle HJ, Luong TN, Medina-Marino A, Schenker L, Khorosheva E, Indersmitten T, Gunapala KM, Steele AD, O'Dell TJ, Patterson PH, Kennedy MB. Deletion of densin-180 results in abnormal behaviors associated with mental illness and reduces mGluR5 and DISC1 in the postsynaptic density fraction. J Neurosci . 2011 Nov 9 ; 31(45):16194-207. PubMed Abstract

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Comment by:  Anand Gururajan
Submitted 12 January 2012 Posted 19 January 2012

Comment by Anand Gururjan, Rachel Hill, and Maarten van Den Buuse
Reverse-engineering clinical abnormalities in rodents has been a standard approach to creating models of aspects of psychiatric illness, but with the use of genetic knockouts, we have managed to achieve a level of resolution not previously seen using classical drug-induced, lesion-induced, or neurodevelopmental models. Indeed, the use of knockouts in combination with these techniques would, in theory, provide a more accurate model. However, before such combinations are trialed, we would necessarily need to establish the robustness of the knockout model by itself in terms of its construct and face and predictive validity.

As outlined by Carlisle et al. (2011), a model has been created based on clinical findings that genetic variations in the components of the post-synaptic density fraction (PSD) have been linked to several psychiatric disorders. The PSD machinery plays a very important role in regulating signal strength and also selectivity of signals...  Read more

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