Aging-related motor function and dopaminergic neuronal loss in C57BL/6 mice

• Published in: Molecular brain Vol. 13; no. 1; p. 46
• Main Authors: Noda, Sachiko, Sato, Shigeto, Fukuda, Takahiro, Tada, Norihiro, Hattori, Nobutaka
• Format: Journal Article
• Language: English
• Published: England BioMed Central Ltd 23.03.2020; BioMed Central; BMC
• Subjects: Age; Aging; Aging - pathology; Animals; Brain; Brain - pathology; C57BL/6 mouse; Chromatography; Disabilities; Diseases; Dopamine; Dopamine receptors; Dopaminergic neuron; Dopaminergic Neurons - pathology; High performance liquid chromatography; House mouse; Liquid chromatography; Mice, Inbred C57BL; Micro Report; Mitochondria; Mitochondrial DNA; Motor Activity; Movement disorders; Musculoskeletal system; Neostriatum; Nervous system diseases; Neurodegenerative diseases; Neurons; Parkinson's disease; Phenols (Class of compounds); Phenotypes; Rotarod Performance Test; Time; C57BL/6 mouse; Aging; Dopaminergic neuron; Mitochondria
• ISSN: 1756-6606; 1756-6606
• DOI: 10.1186/s13041-020-00585-6

Aging-related dopaminergic neuronal loss and its motor phenotypes are well known. Excessive loss of dopaminergic neurons leads to Parkinson's disease (PD), the most common neurodegenerative disorder characterized by the loss of nigrostriatal dopamine-producing neurons. In mice, however, aging-related dopaminergic neuronal loss and its consequences for motor function are poorly understood. We observed the phenotype of wild-type C57BL/6 mice over an extended period of time. C57BL/6 mice exhibited age-dependent locomotor impairments, including hindlimb defects and the number of dopaminergic neurons decreased in aged mice, contributing to locomotor dysfunction. We observed a reduction in striatal dopamine levels in aged mice using high-performance liquid chromatography (HPLC). Thus, dopamine levels are affected by the loss of dopaminergic neurons. Furthermore, fragmented mitochondria were observed in dopaminergic neurons of aged mice but not in those of young mice. Aging-related dopaminergic neuronal loss and accumulation of damaged mitochondria may underlie the pathophysiology of aging.