THE CONNECTIONAL ORGANIZATION OF THE THALAMUS

University Of Wisconsin Madison, Madison WI

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Abstract

The centromedian nucleus (CM-Pf) projects to striatal (caudate and putamen) neurons that are key components of basal ganglia pathways that regulate movement. It is well documented that diseases involving basal ganglia circuitry result in the debilitating deficits associated with Parkinson s and Huntington s disease, but the role of the CM-PF-striatal projection in these deficits has not been explored. The single hypothesis to be tested is that the projections from the cerebral cortex drive the response properties of CM-Pf neurons. Thus we predict that cortical terminals are closely associated with the inhibitory entopeduncular terminals on the proximal dendrites of CM-PF-striatal neurons. Such a finding would suggest that these excitatory cortical drivers could play a role in determining the amount of inhibition flowing out of the basal ganglia (entopeduncluar nucleus). Disease involving the nigrostriatal dopaminergic pathway results in increased inhibition flowing out of the basal ganglia to the motor thalamus and, in turn, the motor cortex. One possible way of turning up the amount of excitation reaching striatal neurons would be to increase the firing of the CM-PF-striatal excitatory projection via the excitatory cortical driver. This could ultimately lower the amount of inhibition leaving the basal ganglia for the motor thalamus and possible help to alleviate some of the Parkinsonian deficits. The fining that cortex is driving CM-PF neurons would modify and extend current models in which the outflow of the basal ganglia is thought to dominate CM-PF function. If Rls in CM-Pf come from the cortex, and share the major synaptic relationships of primary afferents in other thalamic nuclei, we will have a strong argument for changing contemporary views regarding the functions of the CM-Pf (and possibly other intralaminar nuclei) and its role in motor activity. Our findings will be incorporated into current models of basal ganglia circuits, which themselves have shortcomings that necessitate revisions and updating (Wichmann and DeLong 96).