[The consequences of sodium pump inhibition in the neurons and its relevance to the physiopathology of the cell damage produced by anoxic ischemia].

The effect of altering the transmembrane electrochemical Na+ gradient on total membrane conductance (Gm) of Helix aspersa neurones was investigated with intracellular microelectrode recording techniques. Replacement of extracellular Na+ with an impermeant cation (glucamine) produced a modest and short lived decrease in Gm (4.6 +/- 2.9%) followed by a prominent and sustained increase of it (30.3 +/- 10.5%). The latter effect was accompanied by membrane hyperpolarization. These results suggest that removal of external Na+ leads to an increase in [Ca++]i probably through the Na+/Ca++ exchanger operating in reverse mode. The resulting rise in [Ca++]i would be sufficient to produce an increase in membrane permeability to K+. Inhibition of the Na+ pump with ouabain results in a similar increase in Gm, suggesting a rise in [Ca++]i through the Na+/Ca++ exchanger and voltage-sensitive Ca++ channels. Mathematical modelling of Na+/Ca++ exchange in these neurones showed that modest increments in [Na+]i produce significant increases in [Ca++]i in agreement with [Na+]i and [Ca++] measurements performed with fluorescent indicators and ion-selective microelectrode techniques. The results are discussed in relation with the cellular changes occurring in ischemic-anoxic nervous tissue.