These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Sodium-bicarbonate cotransport current in identified leech glial cells.
    Author: Munsch T, Deitmer JW.
    Journal: J Physiol; 1994 Jan 01; 474(1):43-53. PubMed ID: 8014897.
    Abstract:
    1. The membrane current associated with the cotransport of Na+ and HCO3- was investigated in neuropil glial cells in isolated ganglia of the leech Hirudo medicinalis L. using the two-electrode voltage-clamp technique. 2. The addition of 5% CO2-24 mM HCO3- evoked an outward current, which slowly decayed, and which was dependent upon the presence of external Na+. Removal of CO2-HCO3- elicited a transient inward current. Re-addition of Na+ to Na(+)-free saline in the presence of CO2-HCO3- also produced an outward current. Under these conditions an intracellular alkalinization and a rise in intracellular [Na+] were recorded using triple-barrelled, ion-sensitive microelectrodes. Addition or removal of HCO3-, in the absence of external Na+, caused little or no change in membrane voltage, membrane current and intracellular pH, indicating that the glial membrane has a very low HCO3- conductance. 3. Voltage steps revealed nearly linear current-voltage relationships both in the absence and presence of CO2-HCO3-, with an intersection at the assumed reversal potential of the HCO(3-)-dependent current. These results suggest a cotransport stoichiometry of 2HCO3-: 1 Na+. The HCO(3-)-dependent current could be inhibited by diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS). 4. Simultaneous recording of current and intracellular pH showed a correlation of the maximal acid-base flux with the transient HCO(3-)-dependent current during voltage steps in the presence of CO2-HCO3-. The maximum rate of acid-base flux and the HCO(3-)-dependent peak current showed a similar dependence on membrane voltage. Lowering the external pH from 7.4 to 7.0 produced an inward current, which increased twofold in the presence of CO2-HCO3-. This current was largely inhibited by DIDS, indicating outward-going electrogenic Na(+)-HCO3- cotransport during external acidification. 5. When external Na+ was replaced by Li+, a similar outward current and intracellular alkalinization were observed in the presence of CO2-HCO3-. The Li(+)-induced intracellular alkalinization was not inhibited by amiloride, a blocker of Na+(Li+)-H+ exchange, but was sensitive to DIDS. These results suggest that Li+ could, at least partly, substitute for Na+ at the cotransporter site. 6. Our results indicate that the Na(+)-HCO3- cotransport produces a current across the glial cell membrane in both directions with a reversal potential near the membrane resting potential, rendering pHi a function of the glial membrane potential.
    [Abstract] [Full Text] [Related] [New Search]