The Basal Ganglia: More than just a switching device

Abstract

The basal ganglia consist of a variety of subcortical nuclei engaged in motor control and executive functions, such as motor learning, behavioral control, and emotion. The striatum, a major basal ganglia component, is particularly useful for cognitive planning of purposive motor acts owing to its structural features and the neuronal circuitry established with the cerebral cortex. Recent data indicate emergent functions played by the striatum. Indeed, cortico-striatal circuits carrying motor information are paralleled by circuits originating from associative and limbic territories, which are functionally integrated in the striatum. Functional integration between brain areas is achieved through patterns of coherent activity. Coherence belonging to cortico-basal ganglia circuits is also present in Parkinson's disease patients. Excessive synchronization occurring in this pathology is reduced by dopaminergic therapies. The mechanisms through which the dopaminergic effects may be addressed are the object of several ongoing investigations. Overall, the bulk of data reported in recent years has provided new vistas concerning basal ganglia role in the organization and control of movement and behavior, both in physiological and pathological conditions. In this review, basal ganglia functions involved in the organization of main movement categories and behaviors are critically discussed. Comparatively, the multiplicity of Parkinson's disease symptomatology is also revised.

Juvenile stress causes reduced locomotor behavior and dendritic spine density in the prefrontal cortex and basolateral amygdala in Sprague–Dawley rats

“…Together, with reduced locomotion at pre and postpubertal ages, the pyramidal neurons of the PFC also exhibited reduced dendritic length at the same ages. Consequently, it is possible to suggest that reduced dendritic length of the PFC decreased the excitatory input to the striatum, reducing the gabaergic entry to the globus pallidus, which causes an increase in the inhibitory gabaergic output to the thalamus that results in a reduction in the motor cortex activity (for review see Flores, Morales‐Medina, & Diaz, , Florio et al, ).…”

Compensatory Relearning Following Stroke: Cellular and Plasticity Mechanisms in Rodents

“…Crossed cortico-striatal projections are only ≈20% of the total afferents to the contralateral striatum (Smith et al, 2016), but massive collateral sprouting from this minor projection would still be representative (Uryu et al, 2001). Interestingly, crossed cortico-striatal neurons preferentially make synapses with dMSNs, while cortico-striatal neurons with iMSNs (Cowan and Wilson, 1994; Florio et al, 2018). This suggests that the increased post-stroke crossed cortico-striatal inputs would favor movement disinhibition in the ipsilesional motor system.…”

GPRIN3 Controls Neuronal Excitability, Morphology, and Striatal-Dependent Behaviors in the Indirect Pathway of the Striatum

“…Considering the multitude of functions played by the striatum, MSNs are the target not only of dopamine, but also other endogenous G-protein-regulating neuromodulators, such as serotonin, cannabinoids, adenosine, and opioids, since the control of many functions is dependent on multiple synchronized ligand actions (Augusto et al, 2013;Araque et al, 2017;Cavaccini et al, 2018;Nummenmaa et al, 2018). The malfunction of this intricate machinery translates into several striatum-related pathologies, such as addiction, Huntington's disease, Parkinson's disease, depression, and schizophrenia, among others (Li et al, 2015;Florio et al, 2018;Rivas-Grajales et al, 2018). It is still debatable how GPCRs fine-tune the signaling between the binding of certain neuromodulators and the subsequent molecular mechanisms.…”