Cholecystokinin (CCK) increases intracellular calcium in nodose neurons in short term culture

CCK inhibits gastric emptying, acid secretion and stimulates pancreatic function in the postprandial period by an action on the vagal sensory pathway. In order to determine whether CCK directly stimulates vagal afferent neurons from the upper gastrointestinal tract, nodose ganglia were removed from rats in which the stomach or intestine was injected 15-20 days previously with a retrograde tracer (10 ul of 10% solution of dextran conjugated Texas Red) and neurons cultured using standard techniques. Intracellular calcium ([Ca2+]i) was measured in Fura-2 labelled neurons using a videomicroscopic imaging system. Superfusion with CCK (0.1 -10 uM) resulted in a rapid and short-lasting increase in [Ca2+]i that returned to baseline within 2 mins. Capsaicin (300 nM) also increased [Ca2+]i in nodose neurons; this rise was rapid and long-lasting. CCK increased [Ca2+]i in 5/15 capsaicin-sensitive neurons; only 1/15 capsaicin-insensitive neurons responded to CCK. Conclusion: CCK stimulates functional CCK receptors on capsaicin-sensitive vagal afferent neurons innervating the gastrointestinal tract.