The rules governing the assembly of GABA(A) receptors in vivo were assessed in subunit mutant mice. The transcription of individual subunit genes was regulated independently. The lack of a particular subunit did not result in a molecular rescue by an enhanced transcription of other subunits. In addition, the availability of an alpha- and beta-subunit was essential for receptor formation. Finally, highly selective recognition processes directed the subcellular targeting of receptors. The loss of a particular receptor subtype (alpha5) did not lead to a subcellular redistribution of the remaining subtype (alpha2) present in the same cell.