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. During the past funding period, efforts have been devoted towards the understanding of the role GABA transporters (GATs) may play in regulating GABA-B receptors activation in the pallidal complex of normal and parkinsonian nonhuman primates. These experiments were complemented with in vitro electrophysiological studies in rat brain slices to further understand the synaptic mechanisms by which GAT blockade modulates activity of pre- and postsynaptic GABA-B receptors in the globus pallidus. The following conclusions can be made from these studies: (1) The localization of the GABA-BR1 subunit of the GABA-B receptor in GPe and GPi was similar in parkinsonian and normal monkeys. However, the reduction in firing in GPe and GPi produced by microinjections of the GABA-B receptor agonist baclofen was larger in MPTP-treated animals than in normal monkeys, and injections of the GABA-B receptor antagonist CGP55845A produced more commonly decreased firing in GPi in the parkinsonian than in the normal animals. In addition, the injections of baclofen in GPe and GPi, or of CGP55845A in GPi lead to a significant increase in the proportion of spikes in rebound bursts in parkinsonian animals, but not in normal monkeys. Thus, GABA-B receptor mediated transmission is altered in GPi and may contribute to bursting activities in the parkinsonian state. (2) In vitro, GAT inhibitors significantly prolonged the decay time, but did not affect the amplitude, of eIPSCs induced by striatal stimulation (15-20 volts) in the rat GP. These data indicate that GAT-1 and GAT-3 represent differential target sites through which GABA reuptake may subserve complementary regulation of GABAergic transmission in the rat GP.

National Institute of Health (NIH)
National Center for Research Resources (NCRR)
Primate Research Center Grants (P51)
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Special Emphasis Panel (ZRR1-CM-5 (01))
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Emory University
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