The distribution of 13 GABAA receptor subunit mRNAs in the rat brain

Laboratory of Molecular Neuroendocrinology, Zentrum für Molekulare Biologie, University of Heidelberg, Germany.
The Journal of Neuroscience : The Official Journal of the Society for Neuroscience (Impact Factor: 6.34). 04/1992; 12(3):1040-62.
Source: PubMed


The expression patterns of 13 GABA A receptor subunit encoding genes (α1-α6, β1-β3, γ1-γ3,δ) were determined in adult rat brain by in situ hybridization. Each mRNA displayed a unique distribution, ranging from ubiquitous (α1 mRNA) to narrowly confined (α6 mRNA was present only in cerebellar granule cells). Some neuronal populations coexpressed large numbers of subunit mRNAs, whereas in others only a few GABAA receptor-specific mRNAs were found. Neocortex, hippocampus, and caudate-putamen displayed complex expression patterns, and these areas probably contain a large diversity of GABAA receptors. In many areas, a consistent coexpression was observed for α1 and β2 mRNAs, which often colocalized with γ2 mRNA. The α1β2, combination was abundant in olfactory bulb, globus pallidus, inferior colliculus, substantia nigra pars reticulata, globus pallidus, zona incerta, subthalamic nucleus, medial septum, and cerebellum. Colocalization was also apparent for the α2 and β3 mRNAs, and these predominated in areas such as amygdala and hypothalamus. The α3 mRNA occurred in layers V and VI of neocortex and in the reticular thalamic nucleus. In much of the forebrain, with the exception of hippocampal pyramidal cells, the α4 and δ transcripts appeared to codistribute. In thalamic nuclei, the only abundant GABAA receptor mRNAs were those of α1, α4, β02, and δ. In the medial geniculate thalamic nucleus, α1, α4, β02, δ and γ3 mRNAs were the principal GABAA receptor transcripts. The α5 and β1, mRNAs generally colocalized and may encode predominantly hippocampal forms of the GABAA receptor. These anatomical observations support the hypothesis that α1,β2γ2 receptors are responsible for benzodiazepine I (BZ I) binding, whereas receptors containing α2,α3, and α5 contribute to subtypes of the BZ II site. Based on significant mismatches between α4/δ and γ mRNAs, we suggest that in vivo, the α4 subunit contributes to GABAA receptors that lack BZ modulation.

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