Voltage‐dependent potassium channels in mouse Schwann cells.

Abstract

SUMMARY1. Ionic currents in Schwann cells cultured from enzymatically dissociated sciatic nerves of newborn mice were recorded by the whole-cell variation of the patch-clamp technique.2. In these cells only the voltage-dependent K+ currents were recorded. The K+ current was suppressed by quinine, 4-aminopyridine (4-AP) or tetraethylammonium (TEA), their half-suppression concentrations being 22 /tM, 0-3 mm and 15 mM, respectively.3. The peak amplitudes and density of the K+ currents in these Schwann cells increased rapidly during the first 2 days of the culture.4. In an investigation of the linkage between K+ channels and Schwann cell proliferation, three different K+ channel blockers (quinine, 4-AP and TEA) were added to the medium at different stages of the culture. In media containing sublethal doses of quinine or 4-AP, the start of cell proliferation was delayed when these drugs were added at 12 h or on day 3. The same doses of these drugs applied on day 6, when the Schwann cells were proliferating, did not affect cell proliferation. TEA showed a discrepancy between the dose-dependent blocking of K+ channels and cell proliferation because of its additional cytotoxic effects.5. It is concluded that voltage-dependent K+ channels in mouse Schwann cells are similar to those observed in human and murine T lymphocytes. These K+ channels are suggested to be involved in Schwann cell proliferation at early stages of development.

Glial potassium channels activated by neuronal firing or intracellular cyclic AMP in Helix.

“…In Schwann cell cultures, the density of voltage-gated K+ channels increases rapidly during the first days of growth and the cell proliferation is delayed by K+ channel blockers (Konishi, 1989). Similar results were observed in Schwann cells from rabbit sciatic nerve explants (Chiu & Wilson, 1989).…”

Voltage‐dependent calcium and potassium channels in Schwann cells cultured from dorsal root ganglia of the mouse.

“…It cannot be assumed immediately that this value is the resting membrane potential (RMP) but it provides an estimate of the actual RMP (Push & Neher. 1987 (Shrager et al 1985), rabbits (Chiu et al 1984) and mice (Konishi, 1989a). In the same preparation as ours, Hoppe et al (1989) reported the presence of voltage-dependent and pH-sensitive K+ currents.…”

“…3B). The current-voltage relationships for these two currents are shown in Fig potential of -30 mV, displayed an inactivation process, called 'cumulative inactivation', similar to those described in molluscan nerve cell bodies (Aldrich, Getting & Thompson, 1979), in human T lymphocytes (DeCoursey, Chandy, Gupta & Cahalan, 1984) and in mouse Schwann cells cultured from sciatic nerves (Konishi, 1989a). In Fig.…”

“…The physiological relevance of such channels, which are similar in many respects to those found in neuronal cells, remains unclear mainly because at the estimated resting membrane potential recorded in different vertebrate Schwann cells (-30 to -50 mV, Gray most of these channels would be largely inactivated. For voltage-dependent K+ channels, Konishi (1989a) concluded that they appeared to be involved in early stages of mouse Schwann cell proliferation. A relationship between Schwann cell proliferation and expression of voltage-dependent K+ channels was also reported for rabbit Schwann cells after nerve transection (Chiu & Wilson, 1989).…”

On the sodium and potassium currents of a human neuroblastoma cell line.

“…Cook, 1988). However, 4-AP has been found to block delayed rectifier currents in human T lymphocytes (DeCoursey, Chandy, Gupta & Cahalan, 1984), in mouse Schwann cells (Konishi, 1989) and in chick calcitonin cells (Kawa, 1988).…”