Frontal lobe dysfunctions in schizophrenia—II. impairments of psychological and brain functions

Levin, Smadar

doi:10.1016/0022-3956(84)90047-5

Cited by 199 publications

(85 citation statements)

References 73 publications

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“…Prefrontal dysfunction have been associated with several psychiatric disorders (Levin, 1984;Weinberger et al, 1992;Zang et al, 2005). The present data suggest that both D1 and D2 receptors within the PFC might have an important role in the neural mechanisms underlying cognitive deficits in such diseases.…”

Section: Prefrontal Cortex Dopamine In Spatial Learningsupporting

confidence: 49%

D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

Rinaldi

Mandillo

Oliverio

et al. 2006

Neuropsychopharmacol

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The prefrontal cortex (PFC) is a cortical area involved in selecting and retaining information to produce complex behaviors. Within the PFC, the dopaminergic system plays an important role in information processing. Thus, the objective of this study was to test whether bilateral administration of the D1 and D2 receptor antagonists in the prelimbic region of the PFC influenced the performance of mice in a non-associative spatial learning task. CD1 mice were bilaterally microinjected in the PFC with either the D1 receptor antagonist, SCH23390 (SCH 6.25; 12.5; 50 ng), or the D2 receptor antagonist, sulpiride (SULP 12.5; 50; 100 ng) and placed into an open field containing five different objects. After three sessions of habituation two objects were repositioned (spatial change) and in the subsequent session one of the objects was substituted (non-spatial change). No significant alteration was observed in the habituation pattern of the animals after D1 or D2 receptor blockade. When two of the objects were displaced, control mice explored the displaced objects far more than the non-displaced ones, while mice treated with SCH or SULP spent a comparable amount of time re-exploring the two object categories. Conversely, DA antagonists had no effects on the discrimination of the new object. Thus, the administration of both SCH and SULP selectively impaired the ability of mice to discriminate a spatial change, without affecting any other behavioral parameter. These findings could provide a model to study the role of the PFC dopaminergic system in spatial learning and to study the neural mechanisms underlying cognitive and attention deficits often observed in psychiatric disorders.

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Section: Prefrontal Cortex Dopamine In Spatial Learningsupporting

confidence: 49%

D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

Rinaldi

Mandillo

Oliverio

et al. 2006

Neuropsychopharmacol

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“…In essence, a paradigm shift had occurred in characterizing chronic schizophrenia as a neurobehavioral disorder particularly involving the frontal lobe (Levin, 1984;Weinberger, Berman, & Zec, 1986) and executive deficits (Goldberg, Weinberger, Berman, Pliskin, & Podd, 1987), rather than a "functional psychosis." At that time, the hypothesis of neurobiological subgroups in schizophrenia was intriguing but not tested.…”

Section: Historical Overview To 1986mentioning

confidence: 99%

Evolving Notions of Schizophrenia as a Developmental Neurocognitive Disorder

Seidman

Mirsky

2017

J Int Neuropsychol Soc

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We review the changing conceptions of schizophrenia over the past 50 years as it became understood as a disorder of brain function and structure in which neurocognitive dysfunction was identified at different illness phases. The centrality of neurocognition has been recognized, especially because neurocognitive deficits are strongly related to social and role functioning in the illness, and as a result neurocognitive measures are used routinely in clinical assessment of individuals with schizophrenia. From the original definitions of the syndrome of schizophrenia in the early 20th century, impaired cognition, especially attention, was considered to be important. Neurocognitive impairments are found in the vast majority of individuals with schizophrenia, and they vary from mild, relatively restricted deficits, to dementia-like syndromes, as early as the first psychotic episode. Neurocognitive deficits are found in the premorbid phase in a substantial minority of pre-teenage youth who later develop schizophrenia, and they apparently worsen by the prodromal, high-risk phase in a majority of those who develop the illness. While there is limited evidence for reversibility of impairments from pharmacological interventions in schizophrenia, promising results have emerged from cognitive remediation studies. Thus, we expect cognitive interventions to play a larger role in schizophrenia in the coming years. Moreover, because youth at risk for schizophrenia can be identified by an emergent high-risk syndrome, earlier interventions might be applied in a preemptive way to reduce disability and improve adaptation. The notion of schizophrenia as a developmental neurocognitive disorder with stages opens up a window of possibilities for earlier interventions. (JINS, 2017, 23, 881-892)

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“…It mediates many critical functions such as planning, regulation of behavior, and drive, which are frequently disturbed in the illness (Fuster, 1980;Levin, 1984;Weinberger, 1988Weinberger, , 1993Young and Fagg, 1990;Weinberger et al, 1994). Schizophrenics exhibit abnormalities in many memory-associated functions mediated by the frontal cortex, such as looseness of associations, impoverished thinking, and difficulty with problem solving.…”

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confidence: 99%

Expression of NMDAR1, GluR1, GluR7, and KA1 Glutamate Receptor mRNAs Is Decreased in Frontal Cortex of “Neuroleptic‐Free” Schizophrenics: Evidence on Reversible Up‐Regulation by Typical Neuroleptics

Sokolov

1998

Journal of Neurochemistry

166

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Schizophrenics exhibit abnormalities in many memory-associated functions mediated by the frontal cortex. Glutamate receptors play key roles in learning and memory. Hence, abnormalities in glutamate receptors within the frontal cortex may be associated with schizophrenia. In addition, emerging evidence indicates that glutamate receptors may be involved in the actions of antipsychotic drugs. To test these hypotheses, we measured mRNAs encoding the NMDAR1, GIuR1, GIuR7, and KA1 subunits of glutamate receptor in the left superior frontal gyrus from 21 elderly schizophrenics with varying histories of antipsychotic drug treatment and nine normal drug-free elderly controls. There were significant negative correlations between NMDAR1, GIuR1, GIuR7, and KA1 mRNA levels and time without neuroleptic medication before death in schizophrenics, indicating that levels of the glutamate receptor mRNAs decline rapidly after drug withdrawal. Further analysis revealed that in "neurolepticfree" (>6 months) schizophrenics, levels of NMDAR1, GluRl, GIuR7, and KA1 mRNA5 were significantly lower than in controls. By contrast, in schizophrenics who were receiving neuroleptics until death, levels of NMDAR1, GIuR1, GIuR7, and KA1 mRNAs did not differ significantly from controls. These findings indicate that decreased levels of NMDAR1, GIuR1, GluR7, and KA1 mRNAs may be present in the frontal cortex of some schizophrenics and that typical neuroleptics may reversibly increase levels of these mRNAs.

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Frontal lobe dysfunctions in schizophrenia—II. impairments of psychological and brain functions

Cited by 199 publications

References 73 publications

D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

D1 and D2 Receptor Antagonist Injections in the Prefrontal Cortex Selectively Impair Spatial Learning in Mice

Evolving Notions of Schizophrenia as a Developmental Neurocognitive Disorder

Expression of NMDAR1, GluR1, GluR7, and KA1 Glutamate Receptor mRNAs Is Decreased in Frontal Cortex of “Neuroleptic‐Free” Schizophrenics: Evidence on Reversible Up‐Regulation by Typical Neuroleptics

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