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Treatment of C6 Glioma Cells and Rats with Antidepressant Drugs Increases the Detergent Extraction of G sα from Plasma Membrane
Author(s) -
Toki Sadamu,
Donati Robert J.,
Rasenick Mark M.
Publication year - 1999
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 - 10.1046/j.1471-4159.1999.0731114.x
Subject(s) - adenylyl cyclase , desipramine , pharmacology , chemistry , glioma , antidepressant , endocrinology , biochemistry , biology , hippocampus , cancer research , enzyme
: Results from previous studies suggested that chronic treatment of rats or C6 glioma cells with antidepressants augments the coupling between G s and adenylyl cyclase. As these effects on C6 glioma cells are seen in the absence of presynaptic input, several antidepressant drugs may have a direct “postsynaptic” effect on their target cells. It was hypothesized that the target of antidepressant action was some membrane protein that may regulate coupling between G proteins and adenylyl cyclase. To test this, C6 glioma cells were treated with amitriptyline, desipramine, iprindole, or fluoxetine for 3 days. Chlorpromazine served as a control for these treatments. Membrane proteins were extracted sequentially with Triton X‐100 and Triton X‐114 from C6 glioma cells. Triton X‐100 extracted more G sα in membranes prepared from antidepressant‐treated C6 glioma cells than from control groups. In addition, cell fractionation studies revealed that the amount of G sα in caveolin‐enriched domains was reduced after antidepressant treatment and that adenylyl cyclase comigrated with G sα in the gradients. These data suggest that some postsynaptic component that increases availability of G s to activate effector molecules, such as adenylyl cyclase, might be a target of antidepressant treatment.