FUNCTIONAL CA2-CELLS CULTURED IN SERUM-FREE MEDIUM - REGULATION BY A DIFFUSIBLE FACTOR FROM NEURONS AND BY CAMP( AND NA+ CHANNELS ON MOUSE SCHWANN)

Citation
C. Beaudulange et al., FUNCTIONAL CA2-CELLS CULTURED IN SERUM-FREE MEDIUM - REGULATION BY A DIFFUSIBLE FACTOR FROM NEURONS AND BY CAMP( AND NA+ CHANNELS ON MOUSE SCHWANN), European journal of neuroscience, 10(5), 1998, pp. 1796-1809
Citations number
57
Categorie Soggetti
Neurosciences
ISSN journal
0953816X
Volume
10
Issue
5
Year of publication
1998
Pages
1796 - 1809
Database
ISI
SICI code
0953-816X(1998)10:5<1796:FCCISM>2.0.ZU;2-A
Abstract
Regulation of expression of functional voltage-gated ion channels for inward currents was studied in Schwann cells in organotypic cultures o f dorsal root ganglia from E19 mouse embryos maintained in serum-free medium. Of the Schwann cells that did not contact axons, 46.5% express ed T-type Ca2+ conductances (I-CaT) TWO days or more after excision of the ganglia, and consequent disappearance of neurites, I-CaT were det ectable in only 10.9% of the cells, and the marker 04 disappeared. On Schwann cells deprived of neurons, T- (but not L-) type Ca2+ conductan ces were re-induced by weakly hydrolysable analogues of cAMP, and by f orskolin tan activator of adenylyl cyclase) after long-term treatment (4 days). With CPT cAMP (0.1-2 mM), 8Br cAMP, db cAMP or forskolin (0. 01 or 0.1 mM), the proportion of cells with I-CaT was not significantl y different from the proportion in the cultures with neurons. These ag ents also induced expression in some cells of tetrodotoxin-resistant N a+ currents, which were rarely induced by neurons, but 04 was not re-i nduced by cAMP analogue treatments that re-induced I-CaT. Inward curre nts (Ba2+ or Na+) were partly restored (P < 0.05) on Schwann cells cul tured for 6-7 days beneath a filter bearing cultured neurons. In contr ast, addition of neuron-conditioned medium was ineffective. The result s suggest that neurons activate, via diffusible and degradable factors , a subset of Schwann cell cAMP pathways leading to expression of I-Ca T, and activate additional non-cAMP pathways that lead to expression o f 04.