Relationship between axonal collateralization and neuronal degeneration in basal ganglia.
In this paper we evaluate the hypothesis of a possible link between the degree of axonal collateralization of neurons located within the different components of basal ganglia and the vulnerability of these neurons to neurodegenerative or neurotoxic events. Our results stemmed from single-cell labeling experiments in rodents and primates, immunohistochemical study of the dopaminergic nigrostriatal pathway in parkinsonian monkeys, and immunocytological analysis of the human striatum in normal individuals and in patients with Huntington's disease. Our results indicate that projection neurons within virtually all basal ganglia components are endowed with a widespread and highly collateralized axon that yields a fixed number of terminals. Such a high degree of axonal collateralization allows exquisitely precise interactions between the various basal ganglia nuclei. However, the maintenance of this unique morphological trait implies high-energy consumption and renders basal ganglia neurons highly vulnerable to neurodegenerative, metabolic or neurotoxic insults.
Parent
M
M
Centre de recherche Université Laval Robert-Giffard, Beauport, Québec, Canada.
Parent
A
A
D000818:Animals; D001369:Axons / Q000502:physiology*; D001479:Basal Ganglia / Q000166:cytology / Q000473:pathology* / Q000502:physiology; D001921:Brain / Q000473:pathology; D005260:Female; D008252:Macaca fascicularis; D008297:Male; D009410:Nerve Degeneration / Q000473:pathology*; D009434:Neural Pathways / Q000473:pathology; D009474:Neurons / Q000502:physiology*; D010302:Parkinson Disease, Secondary / Q000473:pathology; D017729:Presynaptic Terminals / Q000473:pathology; D051381:Rats; D017207:Rats, Sprague-Dawley