The GABA(B) receptor subunits R1 and R2 interact differentially with the activation transcription factor ATF4 in mouse brain during the postnatal development.

Gamma-aminobutyric acid type B receptors (GABA(B)R) belong to the family of G-protein-coupled receptors that mediate synaptic actions by modulation of different ion channels. Here, we demonstrate that the receptor subunits GABA(B)R1 and GABA(B)R2 interact directly with the soluble activating transcription factor 4 (ATF4) in different regions of the neonatal mouse brain. We found that about 5-12% of expressed ATF4 protein is involved in the complex formation with GABA(B) receptors. Confocal fluorescence microscopy showed that GABA(B)R and ATF4 are co-localized in several well-defined spots in neurons and in glial cells. Co-immunoprecipitation analysis also reveals that the interaction efficiency between GABA(B) receptors and ATF4 in the mouse brain markedly changed during postnatal development, and such changes in interaction were dependent on the GABA(B) receptor subtype.