The distribution and morphology of prefrontal cortex pyramidal neurons identified using anti-neurofilament antibodies SMI32, N200 and FNP7. Normative data and a comparison in subjects with schizophrenia, bipolar disorder or major depression

Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes are generally modest and have not always been replicated. We investigated the possibility that specific pyramidal neuron sub-populations, def...

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Published inJournal of psychiatric research Vol. 37; no. 6; pp. 487 - 499
Main Authors Law, Amanda J., Harrison, Paul J.
Format Journal Article
LanguageEnglish
Published Oxford Elsevier Ltd 01.11.2003
Elsevier
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Abstract Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes are generally modest and have not always been replicated. We investigated the possibility that specific pyramidal neuron sub-populations, defined by their immunoreactivity with the anti-neurofilament antibodies SMI32, N200, and FNP7, are differentially affected in these disorders. First, we assessed the distribution and characteristics of pyramidal neurons labelled by the antibodies in the human dorsolateral prefrontal cortex (Brodmann areas 9, 32, 46), using single and double label immunocytochemistry and immunofluorescence. Three largely separate sub-populations of pyramidal neurons were identified, although with more substantial overlap between SMI32- and FNP7-positive neurons in lamina V. We then determined the density, size and shape of the three pyramidal neuron sub-populations in area 9 in patients with schizophrenia, bipolar disorder, or major depressive disorder, compared to controls ( n=15 in each group). We found a lower density of lamina III N200-positive neurons in major depressive disorder than in schizophrenia or bipolar disorder. There were no other overall differences in neuronal density, or in neuronal size or shape, although a planned secondary analysis supported the previously reported decrease of neuronal size in lamina V in bipolar disorder. In summary, our study illustrates a conceptual and methodological approach which may be of value for investigating the differential neuropathological involvement of pyramidal neuron sub-populations. However, we found no clear evidence that the prefrontal neuropathology of schizophrenia or mood disorders preferentially affects SMI32-, N200- or FNP7-immunoreactive pyramidal neurons.
AbstractList Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes are generally modest and have not always been replicated. We investigated the possibility that specific pyramidal neuron sub-populations, defined by their immunoreactivity with the anti-neurofilament antibodies SMI32, N200, and FNP7, are differentially affected in these disorders. First, we assessed the distribution and characteristics of pyramidal neurons labelled by the antibodies in the human dorsolateral prefrontal cortex (Brodmann areas 9, 32, 46), using single and double label immunocytochemistry and immunofluorescence. Three largely separate sub-populations of pyramidal neurons were identified, although with more substantial overlap between SMI32- and FNP7-positive neurons in lamina V. We then determined the density, size and shape of the three pyramidal neuron sub-populations in area 9 in patients with schizophrenia, bipolar disorder, or major depressive disorder, compared to controls ( n=15 in each group). We found a lower density of lamina III N200-positive neurons in major depressive disorder than in schizophrenia or bipolar disorder. There were no other overall differences in neuronal density, or in neuronal size or shape, although a planned secondary analysis supported the previously reported decrease of neuronal size in lamina V in bipolar disorder. In summary, our study illustrates a conceptual and methodological approach which may be of value for investigating the differential neuropathological involvement of pyramidal neuron sub-populations. However, we found no clear evidence that the prefrontal neuropathology of schizophrenia or mood disorders preferentially affects SMI32-, N200- or FNP7-immunoreactive pyramidal neurons.
Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes are generally modest and have not always been replicated. We investigated the possibility that specific pyramidal neuron sub-populations, defined by their immunoreactivity with the anti-neurofilament antibodies SMI32, N200, and FNP7, are differentially affected in these disorders. First, we assessed the distribution and characteristics of pyramidal neurons labelled by the antibodies in the human dorsolateral prefrontal cortex (Brodmann areas 9, 32, 46), using single and double label immunocytochemistry and immunofluorescence. Three largely separate sub-populations of pyramidal neurons were identified, although with more substantial overlap between SMI32- and FNP7-positive neurons in lamina V. We then determined the density, size and shape of the three pyramidal neuron sub-populations in area 9 in patients with schizophrenia, bipolar disorder, or major depressive disorder, compared to controls (n=15 in each group). We found a lower density of lamina III N200-positive neurons in major depressive disorder than in schizophrenia or bipolar disorder. There were no other overall differences in neuronal density, or in neuronal size or shape, although a planned secondary analysis supported the previously reported decrease of neuronal size in lamina V in bipolar disorder. In summary, our study illustrates a conceptual and methodological approach which may be of value for investigating the differential neuropathological involvement of pyramidal neuron sub-populations. However, we found no clear evidence that the prefrontal neuropathology of schizophrenia or mood disorders preferentially affects SMI32-, N200- or FNP7-immunoreactive pyramidal neurons.
Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes are generally modest and have not always been replicated. We investigated the possibility that specific pyramidal neuron sub-populations, defined by their immunoreactivity with the anti-neurofilament antibodies SMI32, N200, and FNP7, are differentially affected in these disorders. First, we assessed the distribution and characteristics of pyramidal neurons labelled by the antibodies in the human dorsolateral prefrontal cortex (Brodmann areas 9, 32, 46), using single and double label immunocytochemistry and immunofluorescence. Three largely separate sub-populations of pyramidal neurons were identified, although with more substantial overlap between SMI32- and FNP7-positive neurons in lamina V. We then determined the density, size and shape of the three pyramidal neuron sub-populations in area 9 in patients with schizophrenia, bipolar disorder, or major depressive disorder, compared to controls (n=15 in each group). We found a lower density of lamina III N200-positive neurons in major depressive disorder than in schizophrenia or bipolar disorder. There were no other overall differences in neuronal density, or in neuronal size or shape, although a planned secondary analysis supported the previously reported decrease of neuronal size in lamina V in bipolar disorder. In summary, our study illustrates a conceptual and methodological approach which may be of value for investigating the differential neuropathological involvement of pyramidal neuron sub-populations. However, we found no clear evidence that the prefrontal neuropathology of schizophrenia or mood disorders preferentially affects SMI32-, N200- or FNP7-immunoreactive pyramidal neurons.Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes are generally modest and have not always been replicated. We investigated the possibility that specific pyramidal neuron sub-populations, defined by their immunoreactivity with the anti-neurofilament antibodies SMI32, N200, and FNP7, are differentially affected in these disorders. First, we assessed the distribution and characteristics of pyramidal neurons labelled by the antibodies in the human dorsolateral prefrontal cortex (Brodmann areas 9, 32, 46), using single and double label immunocytochemistry and immunofluorescence. Three largely separate sub-populations of pyramidal neurons were identified, although with more substantial overlap between SMI32- and FNP7-positive neurons in lamina V. We then determined the density, size and shape of the three pyramidal neuron sub-populations in area 9 in patients with schizophrenia, bipolar disorder, or major depressive disorder, compared to controls (n=15 in each group). We found a lower density of lamina III N200-positive neurons in major depressive disorder than in schizophrenia or bipolar disorder. There were no other overall differences in neuronal density, or in neuronal size or shape, although a planned secondary analysis supported the previously reported decrease of neuronal size in lamina V in bipolar disorder. In summary, our study illustrates a conceptual and methodological approach which may be of value for investigating the differential neuropathological involvement of pyramidal neuron sub-populations. However, we found no clear evidence that the prefrontal neuropathology of schizophrenia or mood disorders preferentially affects SMI32-, N200- or FNP7-immunoreactive pyramidal neurons.
Author Law, Amanda J.
Harrison, Paul J.
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Issue 6
Keywords Psychosis
Bipolar disorder
Connectivity
Morphometry
Immunocytochemistry
Neuropathology
Mood disorder
Human
Central nervous system
Postmortem
Schizophrenia
Depression
Prefrontal cortex
Cell subpopulation
Encephalon
Anatomic pathology
Pyramidal neuron
Comparative study
Language English
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Snippet Alterations in the density and size of pyramidal neurons in the prefrontal cortex have been described in schizophrenia and mood disorder. However, the changes...
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SubjectTerms Adult
Adult and adolescent clinical studies
Antibodies, Anti-Idiotypic - classification
Antibodies, Anti-Idiotypic - immunology
Antibodies, Monoclonal - immunology
Biological and medical sciences
Bipolar disorder
Bipolar Disorder - immunology
Bipolar Disorder - pathology
Cell Count
Connectivity
Depressive Disorder, Major - immunology
Depressive Disorder, Major - pathology
Feasibility Studies
Female
Fluorescent Antibody Technique
Humans
Immunocytochemistry
Immunohistochemistry
Male
Medical sciences
Middle Aged
Miscellaneous
Mood disorders
Morphometry
Nerve Net - immunology
Nerve Net - pathology
Neurofilament Proteins - immunology
Neuropathology
Prefrontal Cortex - immunology
Prefrontal Cortex - pathology
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Psychosis
Pyramidal Cells - immunology
Pyramidal Cells - pathology
Schizophrenia
Schizophrenia - immunology
Schizophrenia - pathology
Title The distribution and morphology of prefrontal cortex pyramidal neurons identified using anti-neurofilament antibodies SMI32, N200 and FNP7. Normative data and a comparison in subjects with schizophrenia, bipolar disorder or major depression
URI https://www.clinicalkey.com/#!/content/1-s2.0-S002239560300075X
https://dx.doi.org/10.1016/S0022-3956(03)00075-X
https://www.ncbi.nlm.nih.gov/pubmed/14563380
https://www.proquest.com/docview/71287023
Volume 37
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