Neural Plasticity in Schizophrenia

Haracz, John L.

doi:10.1093/schbul/11.2.191

Cited by 63 publications

(28 citation statements)

References 348 publications

(420 reference statements)

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“…This allows for the fact that psychomimetic drugs can induce psychotic symptoms and that schizophrenia is primarily a disorder of adulthood. (iii) The abnormality shows a degree of anatomical and neurochemical specificity; the medial temporal lobe (amygdala hippocampus, parahippocampal gyrus and related cortex) and the prefrontal cortex are directly implicated by virtue of their role in learning and memory and their high plastic potential (Haracz, 1985). The fact that these structures have been repeatedly implicated in schizophrenia by functional and structural imaging, cytoarchitectonic and histochemical studies (e.g., Benes et al, 1986;Deakin et al, 1989;Bogerts et al, 1991) is entirely consistent with the current formulation.…”

Section: Explanatory Powersupporting

confidence: 79%

“…The disconnection hypothesis is therefore, implicitly, a dysplastic hypothesis. The aim of this section is identify the particular form of dysplasia that might underlie schizophrenia (see also Haracz, 1985).…”

Section: Connections and Plasticitymentioning

confidence: 99%

“…The regional specificity of plastic potential has also been addressed by looking for the expression of gene products associated with plastic remodelling of neuronal processes. See Haracz (1985) for a review of the experimental evidence relating neural plasticity and schizophrenia.…”

Section: Theoretical Neurobiologymentioning

confidence: 99%

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The disconnection hypothesis

Friston

1998

Schizophrenia Research

791

469

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This article reviews the disconnection hypothesis of schizophrenia and presents a mechanistic account of how dysfunctional integration among neuronal systems might arise. This neurobiological account is based on the central role played by neuronal plasticity in shaping the connections and the ensuing dynamics that underlie brain function. The particular hypothesis put forward here is that the pathophysiology of schizophrenia is expressed at the level of modulation of associative changes in synaptic efficacy; specifically the modulation of plasticity in those brain systems responsible for emotional learning and memory, in the post-natal period. This modulation is mediated by ascending neurotransmitter systems that: (i) have been implicated in schizophrenia; and (ii) are known to be involved in consolidating synaptic connections during learning. The proposed pathophysiology would translate, in functional terms, into a disruption of the reinforcement of adaptive behaviour that is consistent with the disintegrative aspects of schizophrenic neuropsychology.

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Section: Explanatory Powersupporting

confidence: 79%

Section: Connections and Plasticitymentioning

confidence: 99%

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The disconnection hypothesis

Friston

1998

Schizophrenia Research

791

469

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“…The reduction in numbers of neuronal cells was not accompanied by reactive gliosis, as would have been expected for a neurodegenerative lesion occurring in adulthood. Although the cause of the specific cell loss remains unknown, the idea of schizophrenia as a neurodevelopmental disorder is an attractive hypothesis (3,4,(10)(11)(12)(13)(14)(15)(16)(17).…”

mentioning

confidence: 99%

Levels of the growth-associated protein GAP-43 are selectively increased in association cortices in schizophrenia

Perrone‐Bizzozero

Sower

Bird

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

205

100

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The pathophysiology of schizophrenia may involve perturbations of synaptic organization during development. The presence of cytoarchitectural abnormalities that may reflect such perturbations in the brains of patients with this disorder has been well-documented. Yet the mechanistic basis for these features of the disorder is still unknown. We hypothesized that altered regulation of the neuronal growth-associated protein GAP-43, a membrane phosphoprotein found at high levels in the developing brain, may play a role in the alterations in brain structure and function observed in schizophrenia. In the mature human brain, GAP-43 remains enriched primarily in association cortices and in the hippocampus, and it has been suggested that this protein marks circuits involved in the acquisition, processing, and͞or storage of new information. Because these processes are known to be altered in schizophrenia, we proposed that GAP-43 levels might be altered in this disorder. Quantitative immunoblots revealed that the expression of GAP-43 is increased preferentially in the visual association and frontal cortices of schizophrenic patients, and that these changes are not present in other neuropsychiatric conditions requiring similar treatments. Examination of the levels of additional markers in the brain revealed that the levels of the synaptic vesicle protein synaptophysin are reduced in the same areas, but that the abundance of the astrocytic marker of neurodegeneration, the glial fibrillary acidic protein, is unchanged. In situ hybridization histochemistry was used to show that the laminar pattern of GAP-43 expression appears unaltered in schizophrenia. We propose that schizophrenia is associated with a perturbed organization of synaptic connections in distinct cortical associative areas of the human brain, and that increased levels of GAP-43 are one manifestation of this dysfunctional organization.Structural anomalies are present in the brains of patients with schizophrenia. In vivo neuroimaging techniques have demonstrated a significant ventricular enlargement and decrease in cortical mass that seem to be unrelated to the treatment of the disorder (1). Postmortem analyses of schizophrenic patients also show a reduction in the total brain volume, particularly in the cerebral cortex (2). Fine structural neuropathology also has been detected in the frontal and temporal lobes of schizophrenics (reviewed in refs. 3 and 4). Careful microscopic evaluation has revealed specific neuronal loss in the cingulate cortex (5-7), hippocampal formation, entorhinal cortex, and parahippocampal gyrus (8, 9), demonstrating for the first time the presence of cytoarchitectural aberrations in schizophrenia. The reduction in numbers of neuronal cells was not accompanied by reactive gliosis, as would have been expected for a neurodegenerative lesion occurring in adulthood. Although the cause of the specific cell loss remains unknown, the idea of schizophrenia as a neurodevelopmental disorder is an attractive hypothesis (3, 4, 10-17).The presen...

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“…1977]; (4) the hypothesis of linked open sys tems related to the maintenance of schizo phrenia [Strauss and Carpenter, 1977]; (5) the hypothesis of basic disorders related to the subjective experiencing of schizophre nia [Huber et al, 1979], and (6) the hypoth esis of neural plasticity related to the disease process of schizophrenia [Haracz, 1985].…”

Section: A Three-phase Model Of Schizophreniamentioning

confidence: 99%

A Comprehensive View on Affect and Logic

1988

Psychopathology

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Neural Plasticity in Schizophrenia

Cited by 63 publications

References 348 publications

The disconnection hypothesis

The disconnection hypothesis

Levels of the growth-associated protein GAP-43 are selectively increased in association cortices in schizophrenia

A Comprehensive View on Affect and Logic

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