Original Research Article

Galaninergic Innervation of the Cholinergic Vertical Limb of the Diagonal Band (Ch2) and Bed Nucleus of the Stria terminalis in Aging, Alzheimer's Disease and Down's Syndrome
Elliott J. Mufson, Elizabeth Cochran, William Benzing, Jeffrey H. Kordower

Department of Neurological Sciences and Rush Alzheimer's Disease Center, Rush Presbyterian St. Luke's Medical Center, Chicago, Ill., USA

Address of Corresponding Author

Dementia 1993;4:237-250 (DOI: 10.1159/000107329)

  Key Words

• Neurodegeneration
• Plasticity
• Galanin
• Immunohistochemistrv

  Abstract

The galanin (GAL) containing peptide fiber system circuit which innervates acetylcholine containing basal forebrain neurons has been shown to hypertrophy and hyperinnervate remaining cholinergic Ch4 perikarya in Alzheimer's disease (AD). The present study examined whether a similar hyperinnervation occurs within the cholinergic vertical limb of the diagonal band nucleus (Ch2), a portion of the basal forebrain which, unlike Ch4, exhibits only modest degeneration in AD. Furthermore, we evaluated whether GAL hyperinnervation occurs within the basal forebrain in Down's syndrome, a genetic disorder with extensive AD-like pathology including cholinergic basal forebrain neuron degeneration. The present study revealed that virtually all Ch2 neurons were GAL immunonegative. However, this region was innervated by GAL immunoreactive (ir) interneurons and fibers associated with a major galaninergic pathway which travels through the substantia innominata enroute to the hypothalamus, bed nucleus of the stria terminalis as well as vertical limb of diagonal band nucleus. GAL-ir fibers coursing within this fiber bundle hypertrophied in AD relative to age matched controls and the Down's cases. Within the putative Ch2 terminal zones in AD, many of the remaining cholinergic neurons were hyperinnervated by GAL despite the modest reduction in Ch2 neurons. In contrast, GAL-ir fibers were not hypertrophied in Down's syndrome despite extensive cholinergic cell loss within Ch4. Taken together these findings suggest that extensive cholinergic basal forebrain cell loss alone is not sufficient to trigger the basal forebrain GAL plasticity response found in AD.

Copyright © 1993 S. Karger AG, Basel

  Author Contacts

Elliot Mufson, PhD, Department of Neurological Sciences, Tech 2000, 2242 West Harrison, Chicago, IL 60612 (USA)

  Article Information

Accepted: January 5, 1993
Number of Print Pages : 14