4. Concluding Remarks
There is little doubt that the caudal intralaminar nuclei might modulate basal ganglia transmission at mutiple levels. Although thalamostriatal and thalamosubthalamic projections have largely been neglected in most studies dealing with basal ganglia pathophysiology, the data presented here, as well as data coming from other studies, call for a re-evaluation of the position of the thalamic intralaminar nuclei within the basal ganglia model. The anatomical and metabolic data discussed in this communication clearly support the idea that the intralaminar nuclei cannot longer be seen as a simply relay station between the basal ganglia output nuclei and the cortex. The primary, non-dopaminergic neurodegeneration observed in the caudal intralaminar nuclei might play a key role on the pathophysiology of basal ganglia in PD. Indeed, we suggest that the initial neuronal loss observed within CM-Pf may be a kind of self-compensatory mechanism in early stages of dopamine loss.
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Goff, L.KL. et al. (2005). Intralaminar Thalamic Nuclei are Main Regulators of Basal Ganglia. In: Bolam, J.P., Ingham, C.A., Magill, P.J. (eds) The Basal Ganglia VIII. Advances in Behavioral Biology, vol 56. Springer, Boston, MA. https://doi.org/10.1007/0-387-28066-9_31
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