Non-Decaying postsynaptics potentials and delayed spikes in hippocampal pyramidal neurons generated by a zero slope conductance created by the persistent Na+ current

Channels (Austin). 2018 Jan 1;12(1):81-88. doi: 10.1080/19336950.2018.1433940.

Abstract

The negative slope conductance created by the persistent sodium current (INaP) prolongs the decay phase of excitatory postsynaptic potentials (EPSPs). In a recent study, we demonstrated that this effect was due to an increase of the membrane time constant. When the negative slope conductance opposes completely the positive slope conductances of the other currents it creates a zero slope conductance region. In this region the membrane time constant is infinite and the decay phase of the EPSPs is virtually absent. Here we show that non-decaying EPSPs are present in CA1 hippocampal pyramidal cells in the zero slope conductance region, in the suprathreshold range of membrane potential. Na+ channel block with tetrodotoxin abolishes the non-decaying EPSPs. Interestingly, the non-decaying EPSPs are observed only in response to artificial excitatory postsynaptic currents (aEPSCs) of small amplitude, and not in response to aEPSCs of big amplitude. We also observed concomitantly delayed spikes with long latencies and high variability only in response to small amplitude aEPSCs. Our results showed that in CA1 pyramidal neurons INaP creates non-decaying EPSPs and delayed spikes in the subthreshold range of membrane potentials, which could potentiate synaptic integration of synaptic potentials coming from distal regions of the dendritic tree.

Keywords: Zero slope conductance; infinite membrane time constant; non-decaying postsynaptic potential; persistent sodium current; spike latency.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Electric Conductivity
  • Excitatory Postsynaptic Potentials*
  • Hippocampus / cytology*
  • Male
  • Pyramidal Cells / drug effects
  • Pyramidal Cells / metabolism*
  • Rats
  • Rats, Wistar
  • Sodium / metabolism*
  • Tetrodotoxin / pharmacology
  • Voltage-Gated Sodium Channels / metabolism

Substances

  • Voltage-Gated Sodium Channels
  • Tetrodotoxin
  • Sodium

Grants and funding

Work supported by FAPESP (2016/01607-4) grant (to RML) and CNPq (306251/2014-0) grant (to ACR). CCC is a PhD scholarship recipient from CAPES. RFOP is supported by a FAPESP PhD scholarship (grant 2013/25667-8). This work was partially supported by the Research, Innovation and Dissemination Center for Neuromathematics (FAPESP grant 2013/07699-0).