Axonal sodium channels read and transmit input synchrony in local brain circuits

Archive ouverte

Debanne, Dominique | Mickael, Zbili | Rama, Sylvain | Inglebert, Yanis | Boumedine-Guignon, Norah | Fronzaroli-Molinieres, Laure | Russier, Michaël

Edité par CCSD -

International audience. Sensory processing requires mechanisms of fast coincidence-detection to discriminate synchronous from asynchronous inputs. Spike-threshold adaptation enables such a discrimination but is ineffective in transmitting this information to the network. We will discuss unpublished results showing that axonal sodium channels read and transmit precise levels of input synchrony to the postsynaptic cell by modulating the presynaptic action potential (AP) amplitude. In consequence, synaptic transmission is facilitated at connected pairs of L5-L5 synapses when the presynaptic spike is produced by synchronous inputs. Using dual soma-axon whole-cell recordings, calcium imaging, and computer modeling, we show that this facilitation results from enhanced AP amplitude in the axon due to minimized inactivation of sodium channels in the axon. Quantifying global network activity, we found that this process facilitates propagation of synchronous input-mediated spiking activity in local brain circuits and may therefore constitute a powerful code for neuronal computation.

Consulter en ligne

Suggestions

Du même auteur

Axonal Na + channels detect and transmit levels of input synchrony in local brain circuits

Archive ouverte | Zbili, Mickaël | CCSD

International audience. Sensory processing requires mechanisms of fast coincidence detection to discriminate synchronous from asynchronous inputs. Spike threshold adaptation enables such a discrimination but is inef...

Axonal Na + channels detect and transmit levels of input synchrony in local brain circuits

Archive ouverte | Zbili, Mickaël | CCSD

International audience. Detection and transmission of neuronal synchrony in the rat cortex is achieved by fast changes in action potential waveform.

Rescue of Normal Excitability in LGI1-Deficient Epileptic Neurons

Archive ouverte | Extrémet, Johanna | CCSD

International audience. Leucine-rich glioma inactivated 1 (LGI1) is a glycoprotein secreted by neurons, the deletion of which leads to autosomal dominant lateral temporal lobe epilepsy. We previously showed that LGI...

Chargement des enrichissements...