Filaments from the dopamin-ergic neurons in the substantia nigra that transport dopamine into the striatum and other structures of the basal ganglia that require dopamine. In Parkinson’s disease the numbers of these fibers decrease as the numbers of dopamin-ergic neurons diminish, further restricting the supply of dopamine available to facilitate neuro-motor communication. This loss can only be detected at autopsy after death. Scientists consider it one of the defining pathological conditions of Parkinson’s disease. In other neurodegenerative diseases that produce Parkinson’s-like symptoms have normal numbers or nigrostriatal fibers (such as drug induced parkinsonism) or more wide-spread neuronal loss in the basal ganglia in addition to nigrostriatal fiber loss (such as progressive supranuclear palsy [PSP] and multiple system atrophy [MSA]).
There are also filaments from dopaminergic neurons that originate in and transport dopamine from the striatum, called striatonigral fibers as the striatum is their point of origin, toward the substantia nigra and other structures of the basal ganglia. The numbers and apparent function of these fibers remain normal in Parkinson’s disease. However, the striatum does not produce enough dopamine to meet the brain’s needs, and so the normal functioning of striatonigral fibers cannot offset the loss of nigrostriatal fibers. The loss of striatonigral fibers is a characteristic of the Parkinson’s-like disease striatonigral degeneration (SND), which is a component of the multiple system atrophy (MSA) disease complex.
Differentiating between these fibers and their roles in dopamine transport has no therapeutic consequence at present. However, understanding of their functions provides additional insights into the mechanisms of Parkinson’s disease.