CCKB RECEPTOR ACTIVATION RESULTS IN INCREASED [H-3] THYMIDINE INCORPORATION IN RAT GLIOMA C-6 CELLS

Cholecystokinin (CCK) is known to stimulate cell proliferation but inv olvement of CCKB type receptors has not been exactly demonstrated so f ar. We examined the effect of CCK-8S and two receptor agonists on rat glioma C-6 cells when using different CCKB receptor agonists and antag onists. Both CCK-8S and CCKB receptor agonists BC 264 and Suc-Trp-N(Me )Nle-Asp-Phe-NH2 stimulate [H-3]thymidine incorporation. These effects were inhibited by CCKB receptor antagonist L-365,260 over 100-fold mo re effectively than it was seen by using CCKA receptor antagonist L-36 4,718. The data indicate that CCKB receptor agonists are potent stimul ants of rat glioma C-6 cell DNA synthesis suggesting that CCKB recepto r activation is involved in cell proliferation within the central nerv ous system.