Subcellular localization of GABA(B) receptor subunits in rat visual cortex

Although studies in the visual cortex have found gamma -aminobutyric acid B (GABA(B)) receptor-mediated pre- and postsynaptic inhibitory effects on ne urons, the subcellular localization of GABA(B) receptors in different types of cortical neurons and synapses has not been shown directly. To provide t his information, we have used antibodies against the GABA, receptor (R)1a/b and GABA,RB subunits and have studied the localization of immunoreactiviti es in rat visual cortex. Light microscopic analyses have shown that both su bunits are expressed in cell bodies and dendrites of 65-92% of corticocorti cally projecting pyramidal neurons and in 92-100% of parvalbumin (PV)-, cal retinin (CR)-, and somatostatin (SOM)containing GABAergic neurons. Electron microscopic analyses of immunoperoxidase- and immunogold-labeled tissue re vealed staining in the nucleus, cytoplasm and cell surface membranes with b oth antibodies. Colocalization of both subunits was observed in all of thes e structures. GABA(B)R1a/b and GABA(B)R2 were concentrated in excitatory an d inhibitory synapses and in extrasynaptic membranes. In GABAergic synapses , GABA(B)R1a/b and GABA(B)R2 were more strongly expressed postsynaptically on pyramidal and nonpyramidal cells than presynaptically. In type 1 synapse s GABA(B)R1a/b and GABA(B)R2 was found in pre- and postsynaptic membranes. The nuclear localization of GABA(B)R1 and GABA(B)R2 subunits suggests a nov el role for neurotransmitter receptors in controlling gene expression. The synaptic colocalization of GABA(B)R1 and GABA(B)R2 indicates that subunits form heteromeric assemblies of the functional receptor in inhibitory and ex citatory synapses. Subunit coexpression in GABAergic synapses that include PV-containing and PV-deficient terminals suggests that pre- and postsynapti c GABA(B) receptor activation is provided by several different types of int erneurons. The coexpression of both subunits in excitatory synapses suggest s a role for GABA(B) receptors in the regulation of glutamate release and r aises the question how these receptors are activated in the absence of pre- or postsynaptic GABAergic synaptic inputs to excitatory synapses. J. Comp. Neurol. 431:182-197, 2001. (C) 2001 Wiley-Liss. Inc.