Abstract
Gamma-aminobutyric acid B (GABA B) receptors (GBRs) are G-protein-coupled receptors that mediate a slow, prolonged form of inhibition in the basolateral amygdala (ABL) and other brain areas. Recent studies indicate that this receptor is a heterodimer consisting of GABA BR1 (GBR1) and GABA BR2 subunits. In the present investigation, antibodies to the GABA BR1 subunit were used to study the neuronal localization of GBRs in the rat ABL. GBR immunoreactivity was mainly found in spine-sparse interneurons and astrocytes at the light microscopic level. Very few pyramidal neurons exhibited perikaryal staining. Dual-labeling immunofluorescence analysis indicated that each of the four main subpopulations of interneurons exhibited GBR immunoreactivity. Virtually 100% of large CCK+ neurons in the basolateral and lateral nuclei were GBR+. In the basolateral nucleus 72% of somatostatin (SOM), 73% of parvalbumin (PV) and 25% of VIP positive interneurons were GBR+. In the lateral nucleus 50% of somatostatin, 30% of parvalbumin and 27% of VIP positive interneurons were GBR+. Electron microscopic (EM) analysis revealed that most of the light neuropil staining seen at the light microscopic level was due to the staining of dendritic shafts and spines, most of which probably belonged to spiny pyramidal cells. Very few axon terminals (Ats) were GBR+. In summary, this investigation demonstrates that the distal dendrites of pyramidal cells, and varying percentages of each of the four main subpopulations of interneurons in the ABL, express GBRs. Because previous studies suggest that GBR-mediated inhibition modulates NMDA-dependent EPSPs in the ABL, these receptors may play an important role in neuronal plasticity related to emotional learning.
Published Version
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