CHOLECYSTOKININ DEPOLARIZES GUINEA-PIG SPHINCTER OF ODDI NEURONS BY ACTIVATING CCK-A RECEPTORS

Motility studies indicate that cholecystokinin (CCK) acts through a ne ural mechanism in the sphincter of Odd (SO) after meals. To evaluate i ts actions in SO ganglia, CCK was applied by microejection (0.1 mM) or superfusion (0.1 to 300 nM) while recording was carried out intracell ularly from intact SO neurons. In tonic cells, microejection and super fusion of CCK caused a prolonged depolarization accompanied by action potentials. In phasic cells, microejection of CCK caused brief and/or prolonged depolarizations, but superfusion caused only prolonged depol arizations. In afterhyperpolarized cells, CCK did not cause a detectab le change in the resting membrane potential. In low-Na+ Krebs solution , the prolonged depolarizations in both tonic and phasic cells were si gnificantly reduced. Unsulfated CCK (100 nM) had no effect. CCK-induce d depolarization was significantly reduced by a CCK-A, but not a CCK-B , receptor antagonist. It is concluded that CCK can act on CCK-A recep tors to depolarize SO neurons. However, it is unlikely that hormonal C CK could mediate such an action because of the discrepancy between the sensitivity of SO neurons for CCK and the peak concentrations of CCK in the serum after a meal.