Open AccessAction Potential-generating Cells in Human Glioblastomas
Author(s) -
Charalampos Labrakakis,
Stephan Patt,
Patrick Weydt,
J. Cervós-Navarro,
Reinhard Meyer,
Helmut Kettenmann
Publication year - 1997
Publication title -
journal of neuropathology and experimental neurology
Language(s) - Uncategorized
Resource type - Journals
SCImago Journal Rank - 1.441
H-Index - 164
eISSN - 1554-6578
pISSN - 0022-3069
DOI - 10.1097/00005072-199703000-00003
Subject(s) - depolarization , tetrodotoxin , patch clamp , electrophysiology , membrane potential , neuroscience , sodium channel , glioma , current clamp , voltage clamp , ion channel , neuroglia , biology , biophysics , in vitro , chemistry , sodium , central nervous system , receptor , cancer research , biochemistry , organic chemistry
We studied the electrophysiological properties of cells from human glioblastomas obtained after surgery. The membrane currents were compared in cells of acute tissue slices and primary cultures using the whole cell mode of the patch-clamp technique. Very strikingly, in about a third of the tumor cells in situ and in vitro, depolarizing voltage steps elicited large, tetrodotoxin-sensitive inward currents with a threshold of about -30 mV, indicating the presence of voltage-gated sodium channels. In addition, three types of potassium currents, a delayed rectifying, an A-type, and an inward rectifying, were observed. Such a set of voltage-gated channels is characteristic for neurons. Indeed, in these glioblastoma cells, depolarizing current pulses in the current clamp mode were able to generate action potentials with properties similar to those observed in neurons. We interpret this finding as the ability of glioblastoma cells to acquire neuronlike properties but retain some glial features, since they still express markers typical for astrocytes and their precursors. The role of sodium channels in glioblastoma cells is unclear at this moment and needs further investigation. Our findings, however, imply that the tumor tissue can be intrinsically excitable and that neoplastic glial cells themselves may be an etiologic factor for epileptic seizures.