Presynaptic voltage facilitation of synaptic transmission between CA3-CA3 pyramidal neurons

• Autorzy: Bialowas A. , Rama S. , Zbili M. , Fronzaroli-Molinieres L. , Carlier E. , Giraud P. , Debanne D.
• Języki publikacji: EN

Abstrakty

EN

The spread of subthreshold somatic voltage fluctuations into the axon modulates spike-evoked synaptic transmission. In neocortical L5 pyramidal neurons, depolarization-induced facilitation of synaptic efficacy is thought to occur through the enlargement of presynaptic action potential (AP) driven by inactivation of axonal Kv1 potassium channels. We report here in hippocampal slice cultures that synaptic transmission at excitatory CA3-CA3 synapses also depends on the membrane potential of the presynaptic neuron (Vm-pre). In synaptically connected cell-pairs, presynaptic APs produced postsynaptic response recorded in voltage (EPSC) or current-clamp (EPSP) configuration. Synaptic transmission was tested when Vm-pre was held continuously at rest (-61 mV), hyperpolarized (-77 mV) or depolarized potential (-48 mV). The presynaptic voltage facilitation (PVF) of synaptic transmission was quantified by normalizing the postsynaptic responses obtained at -48 mV to those measured at -77 mV. In these conditions, PVF amounted to 135 ± 14% and was associated with a decrease in the paired-pulse ratio. We found that PVF was totally occluded by bath application of the Kv1 channel blocker DTX. Time constant of PVF was determined by evoking single presynaptic APs at increasing delays after the onset of a presynaptic depolarization. The measured time constant (2 s) was compatible with the time constant of the inactivation of D-type current carried by Kv1 channels. Using confocal laser scanning microscopy and Fluo-4 fluorescent calcium indicator, we measured calcium transients in axons of CA3 pyramidal neurons. Depolarization of the cell body from -65 to -50 mV enhanced spike-evoked axonal calcium transients by ~30%. Notably, this facilitation followed the time course of the PVF. We conclude that PVF is a short-term plasticity present at excitatory CA3-CA3 synapses resulting from the increase in spike-evoked calcium transients in the axon caused by voltage-inactivation of Kv1 channels.

• Wydawca: -
• Czasopismo: Acta Neurobiologiae Experimentalis
• Rocznik: 2011
• Tom: 71
• Numer: S
• Opis fizyczny: p.50-51

Twórcy

autor

Bialowas A.

• UMR 641 Laboratoire de Neurobiologie des Canaux Ioniques, INSERM, Universite de la Mediterranee, Marseille, France

autor

Rama S.

• UMR 641 Laboratoire de Neurobiologie des Canaux Ioniques, INSERM, Universite de la Mediterranee, Marseille, France

autor

Zbili M.

• UMR 641 Laboratoire de Neurobiologie des Canaux Ioniques, INSERM, Universite de la Mediterranee, Marseille, France

autor

Fronzaroli-Molinieres L.

• Laboratoire de Neurobiologie des Canaux Ioniques, INSERM U641, Universite de la Mediterranee, Marseille, France

autor

Carlier E.

• UMR 641 Laboratoire de Neurobiologie des Canaux Ioniques, INSERM, Universite de la Mediterranee, Marseille, France

autor

Giraud P.

• UMR 641 Laboratoire de Neurobiologie des Canaux Ioniques, INSERM, Universite de la Mediterranee, Marseille, France

autor

Debanne D.

• UMR 641 Laboratoire de Neurobiologie des Canaux Ioniques, INSERM, Universite de la Mediterranee, Marseille, France

Uwagi

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