Changes in ion channel expression during in vitro differentiation of trout oligodendrocyte precursor cells.

TY - JOUR

T1 - Changes in ion channel expression during in vitro differentiation of trout oligodendrocyte precursor cells.

AU - Glassmeier, Günter

AU - Jeserich, G

PY - 1995

Y1 - 1995

N2 - Voltage-gated ionic currents were studied in cultured trout oligodendrocyte precursor cells derived from larval trout brain with the whole-cell mode of the patch-clamp technique. These bipolar cells which carry the ganglioside epitope A2B5 on their surface differentiated in vitro into immature multipolar oligodendrocytes expressing the myelin glycoprotein IP2, which signifies the initial step of oligodendroglial development in fish CNS. Depolarization above -40 mV activated a fast transient sodium inward current that was eliminated by substituting Na+ for choline and blocked in the presence of 1 microM TTX. The kinetics and the voltage-dependence of inactivation (half-maximal inactivation at -68 mV) resembled those of sodium currents described in mammalian oligodendrocyte precursor cells and CNS neurons. The expression of Na+ channels was developmentally regulated, since high amplitudes were measured only in A2B5+ cells with a characteristic bipolar morphology of glial progenitors. Depolarizing voltage steps, additionally elicited outward potassium currents that were sensitive to external 4-AP. In a subpopulation of cells this outward current consisted of a sustained and a transient component. The amplitude of both components were dependent on the prepulse potential.

AB - Voltage-gated ionic currents were studied in cultured trout oligodendrocyte precursor cells derived from larval trout brain with the whole-cell mode of the patch-clamp technique. These bipolar cells which carry the ganglioside epitope A2B5 on their surface differentiated in vitro into immature multipolar oligodendrocytes expressing the myelin glycoprotein IP2, which signifies the initial step of oligodendroglial development in fish CNS. Depolarization above -40 mV activated a fast transient sodium inward current that was eliminated by substituting Na+ for choline and blocked in the presence of 1 microM TTX. The kinetics and the voltage-dependence of inactivation (half-maximal inactivation at -68 mV) resembled those of sodium currents described in mammalian oligodendrocyte precursor cells and CNS neurons. The expression of Na+ channels was developmentally regulated, since high amplitudes were measured only in A2B5+ cells with a characteristic bipolar morphology of glial progenitors. Depolarizing voltage steps, additionally elicited outward potassium currents that were sensitive to external 4-AP. In a subpopulation of cells this outward current consisted of a sustained and a transient component. The amplitude of both components were dependent on the prepulse potential.

M3 - SCORING: Zeitschriftenaufsatz

VL - 15

SP - 83

EP - 93

JO - GLIA

JF - GLIA

SN - 0894-1491

IS - 1

M1 - 1

ER -