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GABAB receptor auxiliary subunits modulate Cav2.3-mediated release from medial habenula terminals
release_p36jpy3ogvf23dy3ye3okobh5y
by
Pradeep Bhandari,
David Vandael,
Diego Fernández-Fernández,
Thorsten Fritzius,
David Kleindienst,
Cihan Önal,
Jacqueline Montanaro,
Martin Gassmann,
Peter Jonas,
Akos Kulik,
Bernhard Bettler,
Ryuichi Shigemoto
(+1 others)
Published
in eLife
.
2021 Volume 10
Abstract
The synaptic connection from medial habenula (MHb) to interpeduncular nucleus (IPN) is critical for emotion-related behaviors, and uniquely expresses R-type Ca2+ channels (Cav2.3) and auxiliary GABAB receptor (GBR) subunits, the K+-channel tetramerization domain-containing proteins (KCTDs). Activation of GBRs facilitates or inhibits transmitter release from MHb terminals depending on the IPN subnucleus, but the role of KCTDs is unknown. We therefore examined the localization and function of Cav2.3, GBRs, and KCTDs in this pathway in mice. We show in heterologous cells that KCTD8 and KCTD12b directly bind to Cav2.3 and that KCTD8 potentiates Cav2.3 currents in the absence of GBRs. In the rostral IPN, KCTD8, KCTD12b and Cav2.3 co-localize at the presynaptic active zone. Genetic deletion indicated a bidirectional modulation of Cav2.3-mediated release by these KCTDs with a compensatory increase of KCTD8 in the active zone in KCTD12b-deficient mice. The interaction of Cav2.3 with KCTDs therefore scales synaptic strength independent of GBR activation.
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