Izvorni znanstveni članak
Axon morphology of rapid Golgistained pyramidal neurons in the prefrontal cortex in schizophrenia
Ivan Banovac
; Department of Anatomy and Clinical Anatomy, Croatian Institute for Brain Research and Center of Excellence for Basic, Clinical and Translational Neuroscience, University of Zagreb School of Medicine, Zagreb, Croatia
Dora Sedmak
; Department of Anatomy and Clinical Anatomy, Croatian Institute for Brain Research and Center of Excellence for Basic, Clinical and Translational Neuroscience, University of Zagreb School of Medicine, Zagreb, Croatia
Martina Rojnić Kuzman
; University Hospital Centre Zagreb, Zagreb, Croatia
Ana Hladnik
; Department of Anatomy and Clinical Anatomy, Croatian Institute for Brain Research and Center of Excellence for Basic, Clinical and Translational Neuroscience, University of Zagreb School of Medicine, Zagreb, Croatia
Zdravko Petanjek
; ana.hladnik@mef.hr
Sažetak
Aim To analyze axon morphology on rapid Golgi impregnated pyramidal neurons in the dorsolateral prefrontal cortex in schizophrenia.
Methods Postmortem brain tissue from five subjects diagnosed with schizophrenia and five control subjects without neuropathological findings was processed with the
rapid Golgi method. Layer III and layer V pyramidal neurons from Brodmann area 9 were chosen in each brain for
reconstruction with Neurolucida software. The axons and
cell bodies of 136 neurons from subjects with schizophrenia and of 165 neurons from control subjects were traced.
The data obtained by quantitative analysis were compared
between the schizophrenia and control group with the t
test.
Results Axon impregnation length was consistently greater in the schizophrenia group. The axon main trunk length
was significantly greater in the schizophrenia than in the
control group (93.7±36.6 μm vs 49.8±9.9 μm, P=0.032).
Furthermore, in the schizophrenia group more axons had
visibly stained collaterals (14.7% vs 5.5%).
Conclusion Axon rapid Golgi impregnation stops at the
beginning of the myelin sheath. The increased axonal
staining in the schizophrenia group could, therefore, be
explained by reduced axon myelination. Such a decrease
in axon myelination is in line with both the disconnection
hypothesis and the two-hit model of schizophrenia as a
neurodevelopmental disease. Our results support that the
cortical circuitry disorganization in schizophrenia might
be caused by functional alterations of two major classes
of principal neurons due to altered oligodendrocyte development.
Ključne riječi
Hrčak ID:
274622
URI
Datum izdavanja:
31.8.2020.
Posjeta: 358 *