Altered Glutamatergic and GABAergic Mechanisms in the Cingulate Cortex of the Schizophrenic Brain

Beneš, Francine M.

doi:10.1001/archpsyc.1995.03950240033007

Cited by 67 publications

(32 citation statements)

References 29 publications

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“…Involvement of sigma receptors in the action of ketamine is unlikely, because the behavioral effects of ketamine correlate with NMDA, but not sigma, receptor binding affinity (Ginski and Witkin 1994). The presence of glutamatergically mediated psychotomimetic effects of ketamine is also congruent with histological (Benes et al 1991;Benes et al 1992;Benes 1995;Simpson et al 1991;Ishimaru et al 1994;Akbarian et al 1996) and neuroimaging (Bartha et al 1997) evidence for glutamatergic abnormalities in schizophrenia (see also Olney and Farber 1995).…”

mentioning

confidence: 95%

Does Ketamine-Mediated N-methyl-D-aspartate Receptor Antagonism Cause Schizophrenia-like Oculomotor Abnormalities?

Radant

Bowdle

Cowley

et al. 1998

Neuropsychopharmacology

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mentioning

confidence: 95%

Does Ketamine-Mediated N-methyl-D-aspartate Receptor Antagonism Cause Schizophrenia-like Oculomotor Abnormalities?

Radant

Bowdle

Cowley

et al. 1998

Neuropsychopharmacology

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“…Cytoarchitectural anomalies and abnormal distributions of glutamatergic fibers suggest abnormal development of the ECx (Akil and Lewis 1997;Arnold et al 1991;Falkai et al 2000;Beckmann 1986, 1994;Kovalenko et al 2003; but see also Krimer et al 1997;Longson et al 1996). Decreases of synaptic proteins and abnormalities relative to specific neurotransmitter systems have also been detected in the SZ ECx (Bachus et al 1997;Benes 1995;Benes and Berretta 2001;Eastwood et al 1995Eastwood et al , 1997Hemby et al 2002;Mizukami et al 2002;Wolf et al 1995). Surprisingly, very few postmortem microscopic studies have thus far focused on the involvement of the ECx in BD (Law et al 2004;Webster et al 2002).…”

mentioning

confidence: 99%

Parvalbumin Neurons in the Entorhinal Cortex of Subjects Diagnosed With Bipolar Disorder or Schizophrenia

Pantazopoulos¹,

Lange²,

Baldessarini³

et al. 2007

Biological Psychiatry

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“…Microscopic examination of post-mortem brain tissue has led other investigators to postulate that the loss of neurons and/or a developmental deficit, particularly in subregions of the frontal cortex, underlies many core symptoms of schizophrenia (Benes et al, 1991;Benes, 1995;Goldman-Rakic and Selemon, 1997;Lewis, 1997;Goldman-Rakic, 1999). It has been suggested that in at least some cases of schizophrenia, the primary pathological insult may occur in the pre-or perinatal period (Benes et al, 1991;Murray et al, 1992;Pilowski et al, 1993;Goldman-Rakic and Selemon, 1997).…”

mentioning

confidence: 99%

Blockade of Phencyclidine-Induced Cortical Apoptosis and Deficits in Prepulse Inhibition by M40403, a Superoxide Dismutase Mimetic

Wang¹,

McInnis²,

West³

et al. 2003

J Pharmacol Exp Ther

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Repetitive administration of phencyclidine (PCP) in the perinatal period results in cortical apoptosis and a long-lasting deficit in sensorimotor gating. Because these changes are olanzapinesensitive, we have suggested that the effects of perinatal PCP could be used to model certain aspects of schizophrenia. Studies of PCP and N-methyl-D-aspartate-induced cell death suggested that superoxide could play a role in the pathway leading to death after PCP administration. The purpose of the current study was to determine whether the in vivo administration of M40403, a superoxide dismutase mimetic, could prevent PCPinduced cortical apoptosis and/or deficits in prepulse inhibition. Perinatal rat pups were administered 10 mg/kg PCP on postnatal (PN) days 7, 9, and 11 with or without treatment with 10 mg/kg M40403. Pups were either killed on PN 12 for analysis of various apoptotic markers or they were assessed for prepulse inhibition on PN 24 to 26. Treatment with M40403 2 and 24 h after each PCP treatment prevented PCP-induced increases in two measures of apoptosis in the dorsolateral frontal cortex and in the olfactory cortex. PCP-induced proapoptotic changes in Bax and Bcl-X L were also prevented by M40403 treatment. This regimen did not prevent the deficit in prepulse inhibition caused by PCP treatment, but when the treatment regimen was extended through PN 23, M40403 completely prevented the PCP-induced deficit in prepulse inhibition. These data suggest that perinatal PCP treatment leads to long-lasting changes in the pathway(s), leading to cell death and behavioral deficits, and that the superoxide radical plays a critical role in the underlying mechanism.

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Altered Glutamatergic and GABAergic Mechanisms in the Cingulate Cortex of the Schizophrenic Brain

Cited by 67 publications

References 29 publications

Does Ketamine-Mediated N-methyl-D-aspartate Receptor Antagonism Cause Schizophrenia-like Oculomotor Abnormalities?

Does Ketamine-Mediated N-methyl-D-aspartate Receptor Antagonism Cause Schizophrenia-like Oculomotor Abnormalities?

Parvalbumin Neurons in the Entorhinal Cortex of Subjects Diagnosed With Bipolar Disorder or Schizophrenia

Blockade of Phencyclidine-Induced Cortical Apoptosis and Deficits in Prepulse Inhibition by M40403, a Superoxide Dismutase Mimetic

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