The brain stem reticular formation in schizophrenia

Post-mortem brain tissue was obtained from four patients with schizophrenia and five controls to study cell groups in the brain stem reticular formation. Cholinergic neurons in the pedunculopontine nucleus (PPN) and lateral dorsal tegmental nucleus (LDT) were labeled using nicotinamide adenosine din...

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Bibliographic Details
Published in:Psychiatry research 1991-05, Vol.40 (1), p.31-48
Main Authors: Karson, Craig N., Garcia-Rill, Edgar, Biedermann, Joann, Mrak, Robert E., Husain, Muhammad M., Skinner, Robert D.
Format: Article
Language:English
Subjects:
Adult and adolescent clinical studies
Aged
Biological and medical sciences
Brain Mapping - instrumentation
Brain Stem - pathology
brain stem reticular formation
Cell Count
Choline O-Acetyltransferase - analysis
Cholinergic Fibers - pathology
Computer Simulation
Female
Humans
Image Processing, Computer-Assisted - instrumentation
locus ceruleus
Locus Coeruleus - pathology
Male
Medical sciences
Middle Aged
NADPH Dehydrogenase - analysis
Neurons - pathology
pedunculopontine nucleus
Psychology. Psychoanalysis. Psychiatry
Psychopathology. Psychiatry
Psychoses
Reticular Formation - pathology
Schizophrenia
Schizophrenia - pathology
Schizophrenic Psychology
Tyrosine 3-Monooxygenase - analysis
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Summary:Post-mortem brain tissue was obtained from four patients with schizophrenia and five controls to study cell groups in the brain stem reticular formation. Cholinergic neurons in the pedunculopontine nucleus (PPN) and lateral dorsal tegmental nucleus (LDT) were labeled using nicotinamide adenosine dinucleotide phosphate (NADPH)-diaphorase histochemistry, while catecholaminergic neurons of the locus ceruleus (LC) were labeled immunocytochemically using an antibody to tyrosine hydroxylase. In schizophrenic patients, there were increased numbers of neurons in the PPN labeled by NADPH-diaphorase and reduced cell size in the LC. These results implicate the reticular formation as a possible pathophysiological site for at least some patients with schizophrenia. This also suggests that some of the deficits observed may be based on faulty neurodevelopment.
ISSN:0165-1781
1872-7123
DOI:10.1016/0165-1781(91)90143-D