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Acute changes in myo ‐inositol uptake and 22 Na + flux in murine neuroblastoma cells (N1E‐115) following insulin
Author(s) -
Dunlop Marjorie,
Dimitriadis Eva,
Larkins Richard G.
Publication year - 1987
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(87)80880-3
Subject(s) - inositol , flux (metallurgy) , insulin , neuroblastoma , chemistry , radiochemistry , physics , endocrinology , biochemistry , biology , cell culture , genetics , receptor , organic chemistry
myo ‐Inositol uptake was investigated in a murine neuroblastoma clone (N1E‐115) to determine the effect of altered Na + ,K + ‐ATPase activity. The Na + ionophone monensin, and veratridine, an alkaloid affecting voltage‐dependent Na + entry, increased acute 22 Na + uptake and 22 Na + efflux from pre‐loaded cells, concomitant with enhanced myo ‐inositol uptake. This effect was also seen following insulin. Insulin‐stimulated myo ‐inositol uptake was inhibited by amiloride, ouabain and pyrithiamine. Amiloride inhibition suggests that activation of Na + /H + exchange preceding Na + ,K + ‐ATPase activation is involved in insulin stimulation of myo ‐inositol uptake. Pyrithiamine inhibition is an indication of prior activation of the Na + ,K + ‐ATPase α + catalytic subunit by insulin. The results provide evidence that insulin contributes to the maintenance of Na + , K + ‐ATPase in neuronal tissue.