CNS Schwann cells display oligodendrocyte precursor-like potassium channel activation and antigenic expression in vitro.
Central nervous system (CNS) injury triggers production of myelinating Schwann cells from endogenous oligodendrocyte precursors (OLPs). These CNS Schwann cells may be attractive candidates for novel therapeutic strategies aiming to promote endogenous CNS repair. However, CNS Schwann cells have been so far mainly characterized in situ regarding morphology and marker expression, and it has remained enigmatic whether they display functional properties distinct from peripheral nervous system (PNS) Schwann cells. Potassium channels (K+) have been implicated in progenitor and glial cell proliferation after injury and may, therefore, represent a suitable pharmacological target. In the present study, we focused on the function and expression of voltage-gated K+ channels Kv(1-12) and accessory β-subunits in purified adult canine CNS and PNS Schwann cell cultures using electrophysiology and microarray analysis and characterized their antigenic phenotype. We show here that K+ channels differed significantly in both cell types. While CNS Schwann cells displayed prominent K D-mediated K+ currents, PNS Schwann cells elicited K(D-) and K(A-type) K+ currents. Inhibition of K+ currents by TEA and Ba2+ was more effective in CNS Schwann cells. These functional differences were not paralleled by differential mRNA expression of Kv(1-12) and accessory β-subunits. However, O4/A2B5 and GFAP expressions were significantly higher and lower, respectively, in CNS than in PNS Schwann cells. Taken together, this is the first evidence that CNS Schwann cells display specific properties not shared by their peripheral counterpart. Both Kv currents and increased O4/A2B5 expression were reminiscent of OLPs suggesting that CNS Schwann cells retain OLP features during maturation.
Department of Pathology, University of Veterinary Medicine, Bünteweg 17, 30559, Hannover, Germany.
Kristel
K
Kegler
Ilka
I
Imbschweiler
Reiner
R
Ulrich
Peter
P
Kovermann
Christoph
C
Fahlke
Ulrich
U
Deschl
Arno
A
Kalkuhl
Wolfgang
W
Baumgärnter
Konstantin
K
Wewetzer
D000818:Animals; D001464:Barium / Q000494:pharmacology; D055592:Biophysical Phenomena / Q000187:drug effects / Q000502:physiology; D001921:Brain / Q000166:cytology*; D004285:Dogs; D004558:Electric Stimulation; D005732:Gangliosides / Q000378:metabolism; D020869:Gene Expression Profiling; D005904:Glial Fibrillary Acidic Protein; D008564:Membrane Potentials / Q000187:drug effects; D020411:Oligonucleotide Array Sequence Analysis; D018408:Patch-Clamp Techniques; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000737:chemistry / Q000378:metabolism*; D012333:RNA, Messenger / Q000378:metabolism; D020800:Receptor, Nerve Growth Factor / Q000378:metabolism; D012583:Schwann Cells / Q000187:drug effects / Q000502:physiology*; D012584:Sciatic Nerve / Q000166:cytology*; D013433:Sulfoglycosphingolipids / Q000378:metabolism; D019789:Tetraethylammonium / Q000494:pharmacology
D005732:Gangliosides; D005904:Glial Fibrillary Acidic Protein; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D012333:RNA, Messenger; D020800:Receptor, Nerve Growth Factor; D013433:Sulfoglycosphingolipids; C062875:ganglioside A2B5; D001464:Barium; D019789:Tetraethylammonium