Interhemispheric differences of pyramidal cells in the primary motor cortices of schizophrenia patients investigated postmortem

Author:

Szocsics Péter12,Papp Péter3,Havas László45,Lőke János5,Maglóczky Zsófia1

Affiliation:

1. Institute of Experimental Medicine, ELKH Human Brain Research Laboratory, , Budapest 1083 , Hungary

2. Semmelweis University János Szentágothai Doctoral School of Neuroscience, , Budapest 1085 , Hungary

3. Institute of Experimental Medicine, ELKH Cerebral Cortex Research Group, , Budapest 1083 , Hungary

4. Szt. Borbála Hospital Department of Pathology, , Tatabánya 2800 , Hungary

5. Szt. Borbála Hospital Department of Psychiatry, , Tatabánya 2800 , Hungary

Abstract

Abstract Motor disturbances are observed in schizophrenia patients, but the neuroanatomical background is unknown. Our aim was to investigate the pyramidal cells of the primary motor cortex (BA 4) in both hemispheres of postmortem control and schizophrenia subjects—8 subjects in each group—with 2.5–5.5 h postmortem interval. The density and size of the Sternberger monoclonal incorporated antibody 32 (SMI32)-immunostained pyramidal cells in layer 3 and 5 showed no change; however, the proportion of larger pyramidal cells is decreased in layer 5. Giant pyramidal neurons (Betz cells) were investigated distinctively with SMI32- and parvalbumin (PV) immunostainings. In the right hemisphere of schizophrenia subjects, the density of Betz cells was decreased and their PV-immunopositive perisomatic input showed impairment. Part of the Betz cells contained PV in both groups, but the proportion of PV-positive cells has declined with age. The rat model of antipsychotic treatment with haloperidol and olanzapine showed no differences in size and density of SMI32-immunopositive pyramidal cells. Our results suggest that motor impairment of schizophrenia patients may have a morphological basis involving the Betz cells in the right hemisphere. These alterations can have neurodevelopmental and neurodegenerative explanations, but antipsychotic treatment does not explain them.

Funder

National Brain Research Centre

Publisher

Oxford University Press (OUP)

Subject

Cellular and Molecular Neuroscience,Cognitive Neuroscience

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