Dopamine receptor excess and mouse madness.
The dopamine hypothesis of schizophrenia is based on evidence that the major antipsychotic drugs act by blocking dopamine D2 receptors and that dopamine-releasing drugs worsen symptoms. In this issue of Neuron, Kellendonk et al. report an elegant conditional transgenic mouse overexpressing dopamine D2 receptors selectively in the striatum. Strikingly, these animals display selective cognitive impairment typically associated with frontal cortical defects and abnormal dopamine markers in the prefrontal cortex, suggesting that striatal dopamine receptors can influence cortical dopamine function.
Snyder
Solomon H
SH
Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
D000818:Animals; D003072:Cognition Disorders / Q000235:genetics / Q000378:metabolism* / Q000503:physiopathology; D003342:Corpus Striatum / Q000378:metabolism; D004195:Disease Models, Animal; D051379:Mice; D017397:Prefrontal Cortex / Q000502:physiology; D017448:Receptors, Dopamine D2 / Q000235:genetics / Q000378:metabolism*
D017448:Receptors, Dopamine D2