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Desipramine Elicits the Expression of Opiate Receptors and Sulfogalactosylceramide Synthesis in Rat C 6 Glioma Cells
Author(s) -
Tocque Bruno,
Albouz Samia,
Boutry JeanneMarie,
Saux Francoise Le,
Hauw JeanJacques,
Bourdon Raymond,
Baumann Nicole,
Zalc Bernard
Publication year - 1984
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1984.tb12716.x
Subject(s) - desipramine , chemistry , receptor , imipramine , (+) naloxone , cell culture , collagenase , opiate , internalization , biochemistry , pharmacology , endocrinology , antagonist , biology , enzyme , antidepressant , medicine , genetics , alternative medicine , pathology , hippocampus
In the course of our studies on lipidoses induced by amphiphilic drugs, we have investigated the efof desipramine, a tricyclic antidepressant, on glial cells in culture. We noted that the addition of desipramine to the culture medium of C 6 glioma cells resulted in the modification of the lipid profile of the cell membranes. Of particular interest was the presence, in the desipraminetreated cells, of an additional lipid comigrating on thin layer chromatography with Sulfogalactosylceramide (S‐GalCer). Addition of radiolabelled sulfuric acid in the culture medium of the desipramine‐treated cells resulted in the incorporation of [ 35 S]sulfate in the newly synthesized lipid. Furthermore, this lipid was localized selectively by indirect immunofluorescence using a specific rabbit anti‐S‐GalCer antibody on the cell surface of desipraminetreated. but not control, C 6 cells. Desipramine also increased the activity of 3′‐phosphoadenosine‐5′‐phosphosulfate sulfotransferase (the enzyme responsible for the synthesis of S‐GalCer). Since it has been suggested that S‐GalCer may be involved in opiate receptors, we looked for opiate binding sites on C 6 glioma cells after exposure to desipramine. We found that dihydromorphine was able to bind to the desipramine‐treated C 6 cell membrane. The binding of [ 3 H]dihydromorphine (180 fmol/mg protein) was stereospecific and had a K D of 30‐60 n M . Furthermore, morphine reduced both the basal and isoproterenol‐stimulated cyclic AMP levels of the desipraminetreated C 6 cells. This effect was blocked by naloxone. In these respects, the opiate binding sites induced after treatment of C 6 glioma cells with desipramine fulfill the requirements of a true opiate receptor.