An electron microscope immunocytochemical study of GABABR2 receptors in the monkey basal ganglia: A comparative analysis with GABABR1 receptor distribution

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Abstract
Functional γ‐aminobutyric acid (GABA)Breceptors are heterodimers made up of GABABR1 and GABABR2 subunits. The subcellular localization of GABABR2 receptors remains poorly known in the central nervous system. Therefore, we performed an ultrastructural analysis of the localization of GABABR2 receptor immunoreactivity in the monkey basal ganglia. Furthermore, to characterize better the neuronal sites at which GABABR1 and GABABR2 may interact to form functional receptors, we compared the relative distribution of immunoreactivity of the two GABABreceptors in various basal ganglia nuclei. Light to moderate GABABR2 immunoreactivity was found in cell bodies and neuropil elements in all basal ganglia nuclei. At the electron microscope level, GABABR2 immunoreactivity was commonly expressed postsynaptically, although immunoreactive preterminal axonal segments were also frequently encountered, particularly in the globus pallidus and substantia nigra, where they accounted for the third of the total number of GABABR2‐containing elements. A few labeled terminals that displayed the ultrastructural features of glutamatergic boutons were occasionally found in most basal ganglia nuclei, except for the subthalamic nucleus, which was devoid of GABABR2‐immunoreactive boutons. The relative distribution of GABABR2 immunoreactivity in the monkey basal ganglia was largely consistent with that of GABABR1, but some exceptions were found, most noticeably in the globus pallidus and substantia nigra, which contained a significantly larger proportion of presynaptic elements labeled for GABABR1 than GABABR2. These findings suggest the possible coexistence and heterodimerization of GABABR1 and GABABR2 at various pre‐ and postsynaptic sites, but also raise the possibility that the formation of functional GABABreceptors in specific compartments of basal ganglia neurons relies on mechanisms other than GABABR1/R2 heterodimerization. J. Comp. Neurol. 476:65–79, 2004.