Altered emotionality and neuronal excitability in mice lacking KCTD12, an auxiliary subunit of GABAB receptors associated with mood disorders

Cathomas, F; Stegen, M; Sigrist, H; Schmid, L; Seifritz, E; Gassmann, M; Bettler, B; Pryce, C R

doi:10.1038/tp.2015.8

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Cathomas, F., Stegen, M., Sigrist, H., Schmid, L., Seifritz, E., Gassmann, M., Bettler, B., & Pryce, C. R. (2015). Altered emotionality and neuronal excitability in mice lacking KCTD12, an auxiliary subunit of GABAB receptors associated with mood disorders. Translational Psychiatry, 5, e510. https://doi.org/10.1038/tp.2015.8

Abstract

Gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter in the brain, is fundamental to brain function and implicated in the pathophysiology of several neuropsychiatric disorders. GABA activates G-protein-coupled GABAB receptors comprising principal GABAB1 and GABAB2 subunits as well as auxiliary KCTD8, 12, 12b and 16 subunits. The KCTD12 gene has been associated with bipolar disorder, major depressive disorder and schizophrenia. Here we compare Kctd12 null mutant (Kctd12(-/-)) and heterozygous (Kctd12(+/-)) with wild-ty