GABA, GABA transporters, GABAAreceptor subunits, and GAD mRNAs in the rat parabrachial and Kölliker‐Fuse nuclei

Abstract

In the present study, we investigated the key molecules that determine γ-aminobutyric acid (GABA)ergic signal transduction in the parabrachial/Kölliker-Fuse complex (PB/KF) by means of immunocytochemistry and in situ hybridization. Our data demonstrate a dense plexus of GABA-immunoreactive (-ir) varicosities throughout the nuclei of the PB and the KF. The number of neurons expressing GAD65 or GAD67 mRNA was fairly low in the PB, whereas caudally in the KF an accumulation of GAD-expressing neurons was observed. The GABA transporter-3 (GAT-3) was detected in all parts of the PB/KF, whereas immunolabeling for GAT1 was not observed. All nuclei of the PB and the KF exhibited immunoreactivity for the γ2-, α2-, and α3-subunits of the GABAA receptor. γ2-ir was strong and similar in all PB/KF nuclei. In contrast, α2-labeling was particularly intense in the superior lateral PB, and α3-labeling was most prominent in the external lateral and external medial PB, compared with the remaining nuclei. With respect to the subcellular localization, we found γ2-ir in cell bodies and higher order dendrites, whereas α2- and α3-ir was predominantly found in cell bodies. Immunolabeling for the β2/3- and the α1-subunit was seen in cell bodies and presumed dendritic profiles. The staining intensity was strongest in the dorsal lateral PB. Most importantly, the external lateral PB and the waist area were totally devoid of β2/3- and α1-ir. Our data suggest that neural processing in the PB/KF is under a strong GABAergic inhibition that is apparently mediated by different types of GABAA receptors in functionally different pathways through the PB/KF. J. Comp. Neurol. 400:229–243, 1998. © 1998 Wiley-Liss, Inc.