This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.This project's goal is to elucidate the synaptic organization and plasticity of thalamic projections to the striatum in animal models of Parkinson's disease. During the reporting period, we used immunocytochemistry, electron and confocal microscopy, and anterograde axonal tract tracing methods in rats and monkeys. Additionally, we demonstrated a significant increase in the density of corticostriatal, vGluT1-immunoreactive, glutamatergic terminals in the putamen of MPTP-treated monkeys. In contrast, no significant change was found in the density of vGluT2-containing, thalamostriatal afferents, but complex changes in the ratio of axospinous to axodendritic synapses formed by vGluT2-containing was found along the rostrocaudal axis of the caudate nucleus and putamen. These findings demonstrate striking differences in the degree of synaptic plasticity of thalamic and cortical afferents to the striatum in response to dopamine depletion. Knowing that abnormal striatal glutamatergic transmission is a key pathological feature of Parkinsonism, our findings provide further evidence towards a deeper understanding of the sources and mechanisms that underlie this neurochemical anomaly in Parkinson's disease.
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