Proliferative and degenerative changes in striatal spiny neurons in Huntington's disease: a combined study using the section-Golgi method and calbindin D28k immunocytochemistry
Open accessAbstract
Dysmorphic alterations of dendritic arbors and spines in spiny striatal neurons were identified in section-Golgi impregnations of moderate and severe grades of Huntington's disease (HD). These alterations could be characterized as either proliferative or degenerative changes. Proliferative changes included prominent recurving of distal dendritic segments, short-segment branching along dendrites, and increased numbers and size of dendritic spines. Degenerative alterations consisted of truncated dendritic arborizations, occasional focal dendritic swellings, and marked spine loss. Proliferative changes were found primarily in moderate grades of HD, while degenerative changes were predominantly found in severe grades. Cytopathologic changes increased with neuropathologic severity. Similar morphologic alterations were observed in calbindin D28k (Calb) stained neurons in HD striatum. The immunoreactive intensity of Calb staining was increased in the distal dendrites of positive neurons in HD striatum. The present findings provide morphologic and quantitative evidence that confirms an early and marked involvement of spiny striatal neurons in HD and suggest that neuronal growth, rather than degeneration, may be the harbinger of cell death in this disorder.
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The increased white matter and neuropil density alongside striatal volume loss in R6/2 mice might arise from impaired neurite outgrowth or disrupted synapses in Huntington's disease.
“the enhanced white matter and neuropil density coincident with striatal volume loss in R6/2 mice may stem from impaired neurite outgrowth”
From Microglial depletion prevents extracellular matrix changes and striatal volume reduction in a model of Huntington's disease (2020) · cites this paper as Ferrante et al., 1991
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- Authors
- Ferrante, R., Kowall, N., & Richardson, E.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1991-12-01
- Volume
- 11
- Issue
- 12
- Pages
- 3877-3887
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6575286
- OpenAlex
- W1905860502
- Cited by
- 306
- References
- 63
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 8 · 2023: 4 · 2022: 24 · 2021: 17 · 2020: 13 · 2019: 9 · 2018: 8 · 2017: 7 · 2016: 15 · 2015: 11 · 2014: 12 · 2013: 8 · 2012: 17
- FWCI
- 2.09
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r29ns025588-03)
- National Institute of Neurological Disorders and Stroke (NS25588-04)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Genetic Neurodegenerative Diseases
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- Huntington's disease, dendritic spine morphology, dendritic branching, dendritic swelling, calbindin-D28k, neuronal proliferation, neurodegeneration, neuronal growth, cell death
- MeSH terms
- Aged, Aged, 80 and over, Cell Division, Corpus Striatum, Golgi Apparatus, Histological Techniques, Humans, Huntington Disease, Immunohistochemistry, Middle Aged, Molecular Weight, Nerve Degeneration, Neurons, Calbindins, S100 Calcium Binding Protein G, Calbindin 1
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