Medullary catecholaminergic neurons in the normal human brain and in Parkinson's disease

Authors

  • Dr Clifford B. Saper MD, PhD,

    Corresponding author
    1. Department of Pharmacological and Physiological Sciences and Neurology, the Committee on Neurobiology and the Brain Research Institute, University of Chicago, Chicago, IL
    • Department of Pharmacological and Physiological Sciences, University of Chicago, 947 East 58th Street, Chicago, IL 60637
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  • Denise M. Sorrentino MD,

    1. Department of Pharmacological and Physiological Sciences and Neurology, the Committee on Neurobiology and the Brain Research Institute, University of Chicago, Chicago, IL
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  • Dwight C. German PhD,

    1. Departments of Psychiatry and Physiology, University of Texas Southwestern Medical Center, Dallas, TX
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  • Sonsoles De Lacalle MD, PhD

    1. Department of Anatomy, University of Navarra, Pamplona, Spain
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Abstract

Parkinson's disease is thought ot cause degeneration of melanin-pigmented catecholaminergic neurons throughout the brainstem, but little quantitative information is available on the fate of catecholaminergic neurons associated with the dorsal vagal complex or medullary reticular formation. We therefore examined these neurons in the normal human medulla and in the brains of patients with Parkinson's disease, using both a melanin stain and immunohistochemical methods with an antiserum against tyrosine hydroxylase. The greatest numbers of catecholaminergic neurons in the ventrolateral reticular formation (A1/C1 group) were located in the far rostral medulla, whereas the largest populations of catecholaminergic cells in the dorsal vagal complex (A2/C2 group) were found at the level of the area postrema. No loss of cells was observed in the A1/C1 group in the parkinsonian brains. In contrast, the A2/C2 group showed moderate loss of neurons, most marked at the level of the area postrema. This difference was entirely due to the loss of neurons in the medial component of the A2 group, a population that normally is only lightly pigmented, while the heavily pigmented neurons in the ventral and intermediate components of the A2 complex were unaffected. Parkinson's disease causes degeneration only of selected populations of medullary catecholaminergic neurons, without apparent relationship to the extent of melanin pigmentation.

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