Effect of extracellular HCO(3)(-) on Na(+) channel characteristics in hippocampal CA1 neurons

J Neurophysiol. 2000 Nov;84(5):2477-83. doi: 10.1152/jn.2000.84.5.2477.

Abstract

The effect of HCO(3)(-)/CO(2) on membrane properties of isolated hippocampal CA1 neurons was studied with the use of the whole cell configuration of the patch-clamp technique. Neurons were acutely dissociated from 21- to 30-day-old mice. In the current-clamp mode, HCO(3)(-)/CO(2) significantly hyperpolarized CA1 neurons by more than 10 mV and decreased their input resistance. In addition, the overall excitability of these neurons was lower in the presence of HCO(3)(-)/CO(2) than in HEPES. Spontaneous and evoked action potential firing frequency was lower in the presence of HCO(3)(-)/CO(2) than in its absence. In the voltage-clamp mode, both activation and steady-state inactivation of a fast Na(+) current were shifted in the hyperpolarized direction in such a way that the window currents were smaller in HCO(3)(-)/CO(2) than in HEPES. Recovery from inactivation and deactivation from the open state of the fast Na(+) current was slower in HCO(3)(-)/CO(2) than in HEPES. We conclude that HCO(3)(-)/CO(2) decreases the intrinsic excitability of CA1 neurons by altering not only the passive properties of the neuronal membranes but also by changing several characteristics of the fast Na(+) current, including activation and inactivation kinetics as well as the recovery from inactivation and deactivation.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Action Potentials / drug effects
  • Action Potentials / physiology
  • Animals
  • Bicarbonates / pharmacology*
  • Carbon Dioxide / pharmacology
  • Extracellular Space / metabolism
  • Hippocampus / cytology*
  • Hippocampus / physiology
  • Ion Channel Gating / drug effects
  • Ion Channel Gating / physiology
  • Mice
  • Mice, Inbred Strains
  • Neurons / chemistry
  • Neurons / drug effects
  • Neurons / physiology*
  • Patch-Clamp Techniques
  • Sodium / metabolism
  • Sodium Channels / metabolism*
  • Tetrodotoxin / pharmacology

Substances

  • Bicarbonates
  • Sodium Channels
  • Carbon Dioxide
  • Tetrodotoxin
  • Sodium