NMDA hypofunction in the posterior cingulate as a model for schizophrenia: an exploratory ketamine administration study in fMRI

Northoff, Georg; Richter, André; Bermpohl, Felix; Grimm, Simone; Martin, Ernst; Marcar, Valentine L.; Wahl, Constance; Hell, Daniel; Boeker, Heinz

doi:10.1016/j.schres.2004.04.009

Cited by 72 publications

(52 citation statements)

References 53 publications

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“…Most recently, a number of studies investigated the effects of acute ketamine administration on brain response in different cognitive tasks (Honey et al 2004(Honey et al , 2005Northoff et al 2005;Fu et al 2005). In line with our findings, these studies unanimously showed increased ketamine-induced activation in frontal areas involved in episodic memory (Honey et al 2005;Northoff et al 2005), working memory (Honey et al 2004), and verbal fluency (Fu et al 2005).…”

Section: Discussionsupporting

confidence: 89%

Pharmacological modulation of the neural basis underlying inhibition of return (IOR) in the human 5-HT2A agonist and NMDA antagonist model of psychosis

et al. 2008

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The discrepancy between the behavioral and functional imaging outcome indicates that pharmacological fMRI might be a sensitive tool to detect drug-modulated blood oxygenation level-dependent signal changes in the absence of behavioral abnormalities. Our findings might help to further clarify the contradictory findings of IOR in schizophrenic patients and might, thus, shed more light on possible differential pathomechanisms of schizophrenic symptoms.

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Section: Discussionsupporting

confidence: 89%

Pharmacological modulation of the neural basis underlying inhibition of return (IOR) in the human 5-HT2A agonist and NMDA antagonist model of psychosis

et al. 2008

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“…It remains to be determined whether effects extend into adulthood. This demonstration of altered behaviour and hippocampal NMDAR expression is important given that these changes have been implicated in the development of schizophrenia and cognitive impairment in humans (Qin et al 2005;Rowland et al 2005;Northoff et al 2005). That such changes are already detectable in early life may indicate potentially adverse outcomes for the psychiatric health and learning ability of children whose mothers experienced high levels of anxiety during pregnancy or were treated with repeated courses of synthetic glucocorticoid.…”

Section: Discussionmentioning

confidence: 91%

Repeated maternal glucocorticoid treatment affects activity and hippocampal NMDA receptor expression in juvenile guinea pigs

Owen¹,

Matthews

2006

The Journal of Physiology

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The behavioural consequences of prenatal glucocorticoid exposure are not well understood, though emerging studies in humans indicate hyperactivity and altered cognitive development can occur. Further, recent reports indicate that N -methyl-D-aspartate receptors (NMDARs) may mediate the development of postnatal stress behaviours. We hypothesized that prenatal betamethasone (Beta) administration would alter behaviour and the expression of hippocampal NMDAR subunits NR1, NR2A and NR2B in juvenile guinea pig offspring. We found that repeated maternal Beta (1 mg kg −1 ) treatment on gestational days (gd) 40/41, 50/51 and 60/61 (term∼70 days) had no significant effect on birthweight or early growth. However, Beta produced sex-specific effects on open-field activity and hippocampal NMDAR subunit expression compared with controls. Female Beta offspring exhibited significantly increased locomotor activity while there was no effect in Beta males. Beta males exhibited a tendency for decreased anxiety-like behaviour. With respect to NMDAR subunit expression, Beta-exposed females exhibited significantly reduced NR1 mRNA in CA1/2 and CA3 subfields of the hippocampus; there were no effects in Beta males. In conclusion, repeated maternal treatment with Beta, in a similar regimen to that administered to pregnant women at risk of delivering preterm, has profound consequences on behaviour and development of crucial neurotransmitter systems in postnatal life.

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“…Moreover, the PCC (posterior cingulate cortex) which is a crucial node of the default mode network [72] is commonly implicated in schizophrenia [73,74]. …”

Section: The Self Schizophrenia and Brain Midline Regionsmentioning

confidence: 99%

Psychopathology of the Bodily Self and the Brain: The Case of Schizophrenia

Gallese

Ferri

2014

Psychopathology

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In the present paper, we review the recent empirical evidence on the neurobiological basis of a minimal notion of the self, the bodily self. We show the relationship between the body, its motor potentialities and the notion of minimal self. We argue that this approach can shed new light onto self-disturbances and social deficits characterizing schizophrenia. We discuss our approach with other views on the neural correlates of self-disturbances in schizophrenia and propose that cognitive neuroscience can today address the classical topics of psychopathology by adding a new level of description, finally enabling the correlation between the first-person experiential aspects of psychiatric diseases and their neurobiological roots.

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NMDA hypofunction in the posterior cingulate as a model for schizophrenia: an exploratory ketamine administration study in fMRI

Cited by 72 publications

References 53 publications

Pharmacological modulation of the neural basis underlying inhibition of return (IOR) in the human 5-HT2A agonist and NMDA antagonist model of psychosis

Pharmacological modulation of the neural basis underlying inhibition of return (IOR) in the human 5-HT2A agonist and NMDA antagonist model of psychosis

Repeated maternal glucocorticoid treatment affects activity and hippocampal NMDA receptor expression in juvenile guinea pigs

Psychopathology of the Bodily Self and the Brain: The Case of Schizophrenia

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