Abstract
Because of our limited knowledge of the functional role of the thalamostriatal system, this massive network is often ignored in models of the pathophysiology of brain disorders of basal ganglia origin, such as Parkinson’s disease (PD). However, over the past decade, significant advances have led to a deeper understanding of the anatomical, electrophysiological, behavioral and pathological aspects of the thalamostriatal system. The cloning of the vesicular glutamate transporters 1 and 2 (vGluT1 and vGluT2) has provided powerful tools to differentiate thalamostriatal from corticostriatal glutamatergic terminals, allowing us to carry out comparative studies of the synaptology and plasticity of these two systems in normal and pathological conditions. Findings from these studies have led to the recognition of two thalamostriatal systems, based on their differential origin from the caudal intralaminar nuclear group, the center median/parafascicular (CM/Pf) complex, or other thalamic nuclei. The recent use of optogenetic methods supports this model of the organization of the thalamostriatal systems, showing differences in functionality and glutamate receptor localization at thalamostriatal synapses from Pf and other thalamic nuclei. At the functional level, evidence largely gathered from thalamic recordings in awake monkeys strongly suggests that the thalamostriatal system from the CM/Pf is involved in regulating alertness and switching behaviors. Importantly, there is evidence that the caudal intralaminar nuclei and their axonal projections to the striatum partly degenerate in PD and that CM/Pf deep brain stimulation (DBS) may be therapeutically useful in several movement disorders.
Highlights
The evolution of the thalamus and striatum pre-dates the expansion of the cerebral cortex (Butler, 1994; Reiner, 2010; Stephenson-Jones et al, 2011), our knowledge about the functional anatomy and behavioral role of the connections between them is minimal compared to the amount of information that has been gathered about the corticostriatal system (Kemp and Powell, 1971; Alexander et al, 1986; Parent and Hazrati, 1995)
We have recently found a robust loss of CENTER MEDIAN/PARAFASCICULAR (CM/Pf) neurons in monkeys that were chronically treated with low doses of the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), even in motor asymptomatic animals with minimal nigrostriatal dopaminergic denervation (Villalba et al, 2014; Figure 6)
The cloning of vGluT1 and vGluT2 has had a significant impact in our understanding of the anatomical and synaptic organization of the thalamostriatal systems, allowing us to further appreciate that the thalamus is a massive source of extrinsic glutamatergic inputs to the striatum that originates either in the CM/Pf nuclear complex, or in the numerous non-CM/Pf thalamic nuclei
Summary
The cloning of the vesicular glutamate transporters 1 and 2 (vGluT1 and vGluT2) has provided powerful tools to differentiate thalamostriatal from corticostriatal glutamatergic terminals, allowing us to carry out comparative studies of the synaptology and plasticity of these two systems in normal and pathological conditions. Findings from these studies have led to the recognition of two thalamostriatal systems, based on their differential origin from the caudal intralaminar nuclear group, the center median/parafascicular (CM/Pf) complex, or other thalamic nuclei.
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