2011
DOI: 10.1038/npp.2011.181
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Abstract: Glutamate is the primary excitatory neurotransmitter in mammalian brain. Disturbances in glutamate-mediated neurotransmission have been increasingly documented in a range of neuropsychiatric disorders including schizophrenia, substance abuse, mood disorders, Alzheimer's disease, and autism-spectrum disorders. Glutamatergic theories of schizophrenia are based on the ability of N-methyl-D-aspartate receptor (NMDAR) antagonists to induce schizophrenia-like symptoms, as well as emergent literature documenting dist… Show more

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Cited by 822 publications
(648 citation statements)
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References 112 publications
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“…In fact, interactions of glutamatergic NMDAR (N-Methyl-D-Aspartate receptor) and dopamine receptors are a key mechanism in multiple pathophysiological theories of schizophrenia (Frohlich & Van Horn, 2014 Q5 ). NMDARs play a key role in synaptic transmission and in the synaptic plasticity underlying fundamental cognitive functions such as learning and memory (Zorumski & Izumi, 2012) and it has been hypothesized that modulation of plasticity underlying predictive representations is abnormal in schizophrenia (Javitt, 2004;Moghaddam & Javitt, 2012;Stephan, Baldeweg, & Friston, 2006;Stephan, Friston, & Frith, 2009). Beyond predictive processes, there is now much evidence for a general hypofunction of NMDARs in schizophrenia (Coyle, 2012;Heekeren et al, 2008;Stahl, 2007;Umbricht & Krljes, 2005).…”
Section: Schizophreniamentioning
confidence: 99%
“…In fact, interactions of glutamatergic NMDAR (N-Methyl-D-Aspartate receptor) and dopamine receptors are a key mechanism in multiple pathophysiological theories of schizophrenia (Frohlich & Van Horn, 2014 Q5 ). NMDARs play a key role in synaptic transmission and in the synaptic plasticity underlying fundamental cognitive functions such as learning and memory (Zorumski & Izumi, 2012) and it has been hypothesized that modulation of plasticity underlying predictive representations is abnormal in schizophrenia (Javitt, 2004;Moghaddam & Javitt, 2012;Stephan, Baldeweg, & Friston, 2006;Stephan, Friston, & Frith, 2009). Beyond predictive processes, there is now much evidence for a general hypofunction of NMDARs in schizophrenia (Coyle, 2012;Heekeren et al, 2008;Stahl, 2007;Umbricht & Krljes, 2005).…”
Section: Schizophreniamentioning
confidence: 99%
“…While previously, the search for pharmacological targets has largely focused on the dopamine system, recent research has focused on drug targets which impact on glutamatergic and GABAergic neurotransmission [49,50]. In the light of their crucial role in the assuring E/I balance, this approach should be intensified further and may lead to more effective treatments.…”
Section: Summary and Perspectivesmentioning
confidence: 99%
“…Much evidence now suggests that schizophrenia is characterized by both reduced activity at NMDA receptors (Moghaddam & Javitt, 2012;Kantrowitz and Javitt, 2010) and reduced activity in PV containing GABA-ergic neurons . This leads to reduced context-sensitivity and reduced inhibition.…”
Section: Nmdar Function and Gaba-ergic Activity Are Altered In Schizomentioning
confidence: 99%
“…Phillips and Singer, 1997). They are highly expressed on pyramidal cells, and are closely involved in psychotic pathologies characterized by impairments of contextual modulation (Moghaddam and Javitt, 2012;Phillips and Silverstein, 2003;. Furthermore, contextual modulation requires the transmission of a great deal of information, and about 75% of all cortical connections are directly between pyramidal cells (Braitenberg and Schuz, 1991).…”
Section: Modulation That Amplifies Responses To Rf Inputmentioning
confidence: 99%