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The Journal of Neuroscience, February 1, 2003, 23(3):826
Interaction of Calcineurin and Type-A GABA Receptor
 2 Subunits Produces Long-Term Depression at CA1
Inhibitory Synapses
Jian
Wang1, *,
ShuHong
Liu1, *,
Ursula
Haditsch2,
WeiHong
Tu1,
Kimberley
Cochrane1,
Gholamreza
Ahmadian3,
Linda
Tran1,
Jadine
Paw1,
YuTian
Wang3,
Isabelle
Mansuy2,
Michael M.
Salter4, and
YouMing
Lu1
1 Neuroscience Research Group, Department of Physiology
and Biophysics, Faculty of Medicine, University of Calgary, Calgary,
Canada, T2N 4N1, 2 Institute of Cell Biology, Swiss Federal
Institute of Technology, CH-8093 Zürich, Switzerland, and
Departments of 3 Pathology and 4 Physiology,
Programme in Brain and Behaviour, Hospital for Sick Children,
University of Toronto, Toronto, Canada, M5G 1X8
Long-term depression (LTD) is an activity-dependent weakening of
synaptic efficacy at individual inhibitory synapses, a possible cellular model of learning and memory. Here, we show that the induction
of LTD of inhibitory transmission recruits activated calcineurin (CaN)
to dephosphorylate type-A GABA receptor (GABAARs) via the direct binding of CaN catalytic domain to the second
intracellular domain of the GABAAR- 2
subunits. Prevention of the CaN-GABAA receptor complex
formation by expression of an autoinhibitory domain of CaN in the
hippocampus of transgenic mice blocks the induction of LTD. Conversely,
genetic expression of the CaN catalytic domain in the hippocampus
depresses inhibitory synaptic responses, occluding LTD. Thus, an
activity-dependent physical and functional interaction between CaN and
GABAA receptors is both necessary and sufficient for
inducing LTD at CA1 individual inhibitory synapses.
Key words:
GABAA receptors; inhibitory synapses; plasticity; dephosphorylation; calcineurin; hippocampus
*
J.W. and S.L. contributed equally to this work.
Copyright © 2003 Society for Neuroscience 0270-6474/03/233826-11$05.00/0
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