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F M Benes

Publications and source records attributed to F M Benes.

77 records · Page 5Linked to original sources
PubMedDate not supplied

The role of stress and dopamine-GABA interactions in the vulnerability for schizophrenia.

Current hypotheses concerning the etiology of schizophrenia often invoke both an abnormal gene(s) and an environmental disturbance as necessary components to the vulnerability for this disorder. According to one model of schizophrenia presented here, the putative environmental factor may consist of stress and require both pre- and post-natal exposure for a "mis-wiring" of dopaminergic inputs to GABAergic neurons of the cortex to occur. Since the cortical dopamine system continues to mature until the start of the early adult period, the normal ingrowth of dopamine fibers during late adolescence and their formation of aberrant connections with abnormal intrinsic corticolimbic circuits could "trigger" the onset of symptoms in those who carry the constitutional vulnerability for schizophrenia.

Adolescent↗
PubMedDate not supplied

Increased density of glutamate-immunoreactive vertical processes in superficial laminae in cingulate cortex of schizophrenic brain.

Recent postmortem investigations have suggested that schizophrenia may involve a defect in associative information processing in the upper layers of limbic cortex. One of these studies reported that vertical processes visualized with antibodies against the neurofilament 200K subunit (NFP-200K) of the axon cytoskeleton were increased in density in layer II and upper portions of layer IIIa of the cingulate region of schizophrenic individuals. Based on this latter finding, it was hypothesized that there may be a superbundance of associative afferents to this region. To explore this possibility further, an immunoperoxidase localization of the amino acid glutamate has been employed to visualize vertical fibers in layers II and IIIa of postmortem anterior cingulate cortex in both normal controls (n = 15) and schizophrenics (n = 17). Vertical fibers were distinguished according to small or large calibers and were differentially counted with a blind computer-assisted technique. The schizophrenic group showed a markedly higher density (77.8%) of small-caliber glutamate-immunoreactive vertical fibers when compared to controls; the density of large-caliber vertical fibers also showed a similar, though smaller (30.2%), increase in the schizophrenic group. There were no differences in the density of either small- or large-caliber processes in prefrontal cortex of the two groups. The effects of age, postmortem interval, fixation, and neuroleptic exposure do not account for the differences between the normal and schizophrenic subjects. Taking together their small caliber, vertical orientation, localization in superficial layers, and marked glutamate immunoreactivity, it seems plausible that the fibers showing an increased density in schizophrenics may be glutamatergic afferents, possibly ones that are associative in nature.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

The relationship between structural brain imaging and histopathologic findings in schizophrenia research.

The suggestion that schizophrenia may involve a neurodegenerative process has emanated from the highly replicated finding of ventricular enlargement in brain images of patients with this disorder. These investigations have provided a direct impetus for recent histopathologic studies seeking evidence of a neurodegenerative process in the brains of subjects with schizophrenia. Whereas most postmortem studies have reported the presence of atrophy and/or neuronal loss in several corticolimbic regions of subjects with schizophrenia, no quantitative study, to date, has detected an increase in the number of glial cells. For this reason the changes observed in postmortem schizophrenic brain are not consistent with a typical adult pattern of neuronal degeneration, such as that seen in Huntington's disease. Because several studies have reported various changes in layer II of the anterior cingulate, prefrontal, and entorhinal cortices, the histopathologic findings described are compatible with the idea that schizophrenia involves a disturbance of the "inside-out" migration or differentiation of cortical neurons that normally occurs during ontogenesis. A neurodevelopmental perturbation early in life could result in discrete alterations of corticolimbic circuitry that eventually contribute to the appearance of schizophrenic symptoms during adolescence and adulthood.

Adult↗