Abstract
The current model of basal ganglia (BG) was introduced two decades ago and has settled most of our current understanding of BG function and dysfunction. Extensive research efforts have been carried out in recent years leading to further refinement and understanding of the normal and diseased BG. Several questions, however, are yet to be resolved. This short review provides a synopsis of the evolution of thought regarding the pathophysiological model of the BG and summarizes the main recent findings and additions to this field of research. We have also tried to identify major challenges that need to be addressed and resolved in the near future. Detailed accounts and state-of-the-art developments concerning research on the BG are provided in the articles that make up this Special Issue.
Highlights
The basal ganglia (BG) have been traditionally linked to the control of movement. This mindset was mainly derived from early clinico-pathological observations of BG lesions associated with movement disorders and, subsequently, by the profound impact that striatal dopamine (DA) depletion caused both in animals and in patients with Parkinson’s disease (PD)
This process involves the conduction of information from the cerebral cortex and thalamus to the striatum, to the globus pallidus pars interna (GPi) and substantia nigra pars reticulara (SNr), to provide feed-back via the ventral thalamus to the cerebral cortex and the superior colliculus
The first concept was settled on the preponderance of anatomical and neurochemical data available at the time, and based mainly on the fact that different populations of striatal medium spiny neurons (MSNs) project to the output of the BG (GPi and SNr) via “direct” and “indirect” pathways (Alexander et al, 1986; Penney and Young, 1986; Albin et al, 1989; DeLong, 1990)
Summary
The basal ganglia (BG) have been traditionally linked to the control of movement. This mindset was mainly derived from early clinico-pathological observations of BG lesions associated with movement disorders and, subsequently, by the profound impact that striatal dopamine (DA) depletion caused both in animals and in patients with Parkinson’s disease (PD).The first coherent model of the BG was developed in the mid1980s (Penney and Young, 1986; Albin et al, 1989; DeLong, 1990) whereupon the BG were shown to act by integrating and processing information through a series of connections with different brain regions. The first concept was settled on the preponderance of anatomical and neurochemical data available at the time, and based mainly on the fact that different populations of striatal medium spiny neurons (MSNs) project to the output of the BG (GPi and SNr) via “direct” and “indirect” pathways (Alexander et al, 1986; Penney and Young, 1986; Albin et al, 1989; DeLong, 1990).
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