Membrane lipids tune synaptic transmission by direct modulation of presynaptic potassium channels.
Neuron. 2014-02-01; 81(4): 787-799
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Carta M(1), Lanore F(1), Rebola N(1), Szabo Z(1), Da Silva SV(1), Lourenço J(1), Verraes A(2), Nadler A(3), Schultz C(3), Blanchet C(1), Mulle C(4).
(1)University of Bordeaux, Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, 33000 Bordeaux, France.
(2)Institut Jacques Monod, UMR 7592, CNRS and INSERM ERL U950, University Paris Diderot, Sorbonne Paris Cité, 75013 Paris, France.
(3)EMBL Heidelberg, Meyerhofstraße 1, 69117 Heidelberg, Germany.
(4)University of Bordeaux, Interdisciplinary Institute for Neuroscience, CNRS UMR 5297, 33000 Bordeaux, France. Electronic address:
Neuron. 2014 Feb 19;81(4):957.
Neuron. 2014 Feb 19;81(4):717-9.
Nat Rev Neurosci. 2014 Mar;15(3):135.
Voltage-gated potassium (Kv) channels are involved in action potential (AP)
repolarization in excitable cells. Exogenous application of membrane-derived
lipids, such as arachidonic acid (AA), regulates the gating of Kv channels.
Whether membrane-derived lipids released under physiological conditions have an
impact on neuronal coding through this mechanism is unknown. We show that AA
released in an activity-dependent manner from postsynaptic hippocampal CA3
pyramidal cells acts as retrograde messenger, inducing a robust facilitation of
mossy fiber (Mf) synaptic transmission over several minutes. AA acts by
broadening presynaptic APs through the direct modulation of Kv channels. This
form of short-term plasticity can be triggered when postsynaptic cell fires with
physiologically relevant patterns and sets the threshold for the induction of the
presynaptic form of long-term potentiation (LTP) at hippocampal Mf synapses.
Hence, direct modulation of presynaptic Kv channels by activity-dependent release
of lipids serves as a physiological mechanism for tuning synaptic transmission.
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