ANATOMICAL AND PHYSIOLOGICAL CHARACTERIZATION OF THE THALAMOSTRIATAL SYSTEM

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This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. The interaction between the thalamus and the striatum has been implicated in disturbances of basal ganglia function such as Parkinson's disease. Deep brain stimulation of the centromedian/parafascicular (CM/PF) thalamic nuclei is effective in relieving motor symptoms associated with these conditions; however, its therapeutic effects are hampered by the minimal information known about the function of the thalamostriatal system. This study aims to examine the CM/PF-striatal anatomical and functional relationship in nonhuman primates, in order to understand the involvement of the thalamostriatal system in basal ganglia dysfunction. Our findings show that cholinergic interneurons mainly respond to CM activation by decreased activity, which is mediated by the local injection of GABAergic drugs. In the anatomical studies, immunohistochemistry at the electron microscopic level was double-labeled with neuronal markers for medium spiny neurons (MSNs) and striatal cholinergic interneurons (SCIs), in order to determine what portion of the GABAergic inputs observed onto SCIs are derived from MSNs, the main cell group of the striatum. Our findings demonstrate that SCIs mainly receive symmetric synaptic inputs along their entire somatodendritic domain, where MSN collaterals comprise about one quarter of these synaptic inputs. In conclusion, intrastriatal GABAergic microcircuitry is shown to be in a position to play an important role in modulating the responses of SCIs to the activation of the CM in monkeys.