Abstract
Studies in heterologous systems have demonstrated that heterodimerisation of the two GABA B receptor subunits appears to be crucial for the trafficking and signalling of the receptor. Gene targeting of the GABA B1 gene has demonstrated that the expression of GABA B1 is essential for GABA B receptor function in the central nervous system (CNS). However, the contribution of the GABA B2 subunit in the formation of native GABA B receptors is still unclear, in particular whether other proteins can substitute for this subunit. We have created a transgenic mouse in which the endogenous GABA B2 gene has been mutated in order to express a C-terminally truncated version of the protein. As a result, the GABA B1 subunit does not reach the cell surface and concomitantly both pre- and post-synaptic GABA B receptor functions are abolished. Taken together with previous gene deletion studies for the GABA B1 subunit, this suggests that classical GABA B function in the brain is exclusively mediated by GABA B1/2 heteromers.
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