Analog modulation of spike-evoked transmission in CA3 circuits is determined by axonal Kv1.1 channels in a time-dependent manner

Andrzej Bialowas (1) , Sylvain Rama (1) , Mickael Zbili (1) , Vincenzo Marra (1) , Laure Fronzaroli-Molinieres (1) , Norbert Ankri (1) , Edmond Carlier (1) , Dominique Debanne (1)

1 UNIS - Inserm U1072 - Unité de Neurobiologie des canaux Ioniques et de la Synapse

Synaptic transmission usually depends on action potentials (APs) in an all-or-none (digital) fashion. Recent studies indicate, however , that subthreshold presynaptic depolarization may facilitate spike-evoked transmission, thus creating an analog modulation of spike-evoked synaptic transmission, also called analog–digital (AD) synaptic facilitation. Yet, the underlying mechanisms behind this facilitation remain unclear. We show here that AD facilitation at rat CA3–CA3 synapses is time-dependent and requires long presynaptic depolarization (5–10 s) for its induction. This depolarization-induced AD facilitation (d-ADF) is blocked by the specific Kv1.1 channel blocker dendrotoxin-K. Using fast voltage-imaging of the axon, we show that somatic depolarization used for induction of d-ADF broadened the AP in the axon through inactivation of Kv1.1 channels. Somatic depolarization enhanced spike-evoked calcium signals in presynaptic terminals, but not basal calcium. In conclusion, axonal Kv1.1 channels determine glutamate release in CA3 neurons in a time-dependent manner through the control of the presynaptic spike waveform.

Keywords: axon terminal; potassium channels; rat; synaptic plasticity

Domains: Life Sciences [q-bio]; Neurons and Cognition [q-bio.NC]; Neurobiology

Andrzej Bialowas, Sylvain Rama, Mickael Zbili, Vincenzo Marra, Laure Fronzaroli-Molinieres, et al.. Analog modulation of spike-evoked transmission in CA3 circuits is determined by axonal Kv1.1 channels in a time-dependent manner. European Journal of Neuroscience, 2015, 41 (3), pp.293-304. ⟨10.1111/ejn.12787⟩. ⟨hal-01766833⟩