Subcellular localization of GABAB receptor subunits in rat visual cortex

Yuri Gonchar, Liyi Pang, Barbara Malitschek, Bernhard Bettler, Andreas Burkhalter

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63 Scopus citations


Although studies in the visual cortex have found γ-aminobutyric acid B (GABAB) receptor-mediated pre- and postsynaptic inhibitory effects on neurons, the subcellular localization of GABAB receptors in different types of cortical neurons and synapses has not been shown directly. To provide this information, we have used antibodies against the GABAB receptor (R)1a/b and GABABR2 subunits and have studied the localization of immunoreactivities in rat visual cortex. Light microscopic analyses have shown that both subunits are expressed in cell bodies and dendrites of 65-92% of corticocortically projecting pyramidal neurons and in 92-100% of parvalbumin (PV)-, calretinin (CR)-, and somatostatin (SOM)-containing GABAergic neurons. Electron microscopic analyses of immunoperoxidase- and immunogold-labeled tissue revealed staining in the nucleus, cytoplasm and cell surface membranes with both antibodies. Colocalization of both subunits was observed in all of these structures. GABABR1a/b and GABABR2 were concentrated in excitatory and inhibitory synapses and in extrasynaptic membranes. In GABAergic synapses, GABABR1a/b and GABABR2 were more strongly expressed postsynaptically on pyramidal and nonpyramidal cells than presynaptically. In type 1 synapses GABABR1a/b and GABABR2 was found in pre- and postsynaptic membranes. The nuclear localization of GABABR1 and GABABR2 subunits suggests a novel role for neurotransmitter receptors in controlling gene expression. The synaptic colocalization of GABABR1 and GABABR2 indicates that subunits form heteromeric assemblies of the functional receptor in inhibitory and excitatory synapses. Subunit coexpression in GABAergic synapses that include PV-containing and PV-deficient terminals suggests that pre- and postsynaptic GABAB receptor activation is provided by several different types of interneurons. The coexpression of both subunits in excitatory synapses suggests a role for GABAB receptors in the regulation of glutamate release and raises the question how these receptors are activated in the absence of pre-or postsynaptic GABAergic synaptic inputs to excitatory synapses.

Original languageEnglish
Pages (from-to)182-197
Number of pages16
JournalJournal of Comparative Neurology
Issue number2
StatePublished - Mar 5 2001


  • GABA
  • GABA receptor
  • GABAergic synapses
  • Inhibition
  • Slow inhibition


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