期刊
JOURNAL OF COMPARATIVE NEUROLOGY
卷 519, 期 8, 页码 1435-1454出版社
WILEY-BLACKWELL
DOI: 10.1002/cne.22610
关键词
gamma-aminobutyric acid; GABA-B; GABAB; GPCR; KCTD12; KCTD16
资金
- Swiss Science Foundation [3100A0-117816]
- Fridericus Stiftung
- European Community [201714, FP7/2007-2013]
- Deutsche Forschungsgemeinschaft [SFB 746/TP16, SFB 780/A3, EXC294]
GABA(B) receptors are the G-protein-coupled receptors for gamma-aminobutyric acid (GABA). KCTD8, 12, 12b, and 16 were recently identified as auxiliary GABA(B) receptor subunits and distinctly influence biophysical and pharmacological properties of the receptor response. Here we examined the expression patterns of the KCTDs in the mouse brain. Using in situ hybridization analysis, we found that most neurons express KCTD transcripts, supporting biochemical data showing that most GABA(B) receptors in the brain incorporate KCTD proteins. In the adult brain, KCTD12 and 16 have a widespread and KCTD8 and 12b a restricted expression pattern. Individual neurons can coexpress multiple KCTDs, as shown for granule cells and CA1/CA3 pyramidal cells in the hippocampus that coexpress KCTD12 and 16. In contrast, granule, Purkinje, and Golgi cells in the cerebellum selectively express one KCTD at a time. The expression levels of individual KCTD transcripts vary during postnatal brain development. Immunohistochemistry reveals that individual KCTD proteins can exhibit distinct axonal or dendritic localizations in neuronal populations. KCTDs are also detectable in nonneuronal tissues not expected to express GABA(B) receptors, suggesting that the role of KCTD proteins extends beyond GABA(B) receptors. In summary, our findings support that most brain GABA(B) receptors associate with KCTD proteins, but that the repertoire and abundance of KCTDs varies during development, among brain areas, neuronal populations, and at subcellular sites. We propose that the distinct spatial and temporal KCTD distribution patterns underlie functional differences in native GABAB responses. J. Comp. Neurol. 519: 1435-1454, 2011. (C) 2011 Wiley-Liss, Inc.
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