Mercer J G, Farningham D A, Lawrence C B
Rowett Research Institute, Bucksburn, Aberdeen, U.K.
Brain Res. 1992 Jan 13;569(2):311-6. doi: 10.1016/0006-8993(92)90644-o.
Cholecystokinin (CCK) binding sites which accumulate at ligatures placed on the rat vagus nerve may mediate the satiety actions of CCK. Treatment of neonatal rats with capsaicin attenuated the satiety effect of injected CCK in adult life. Capsaicin pretreatment also reduced, but did not eliminate, the accumulation of CCK binding sites proximal and distal to ligatures on either cervical trunk. A similar effect was observed following ligation of subdiaphragmatic vagal trunks. The CCK receptor antagonists, MK-329 and L-365,260, inhibited binding to capsaicin- and vehicle-treated nerves to a similar degree. Densities of CCK binding sites in the nucleus tractus solitarius and area postrema were also markedly affected by neonatal capsaicin treatment.
胆囊收缩素(CCK)结合位点在大鼠迷走神经结扎处聚集,可能介导CCK的饱腹感作用。用辣椒素处理新生大鼠可减弱成年后注射CCK的饱腹感效应。辣椒素预处理也减少了,但并未消除,颈干结扎近端和远端CCK结合位点的积累。在膈下迷走神经干结扎后也观察到类似的效果。CCK受体拮抗剂MK-329和L-365,260对辣椒素处理和未处理神经的结合抑制程度相似。孤束核和最后区CCK结合位点的密度也受到新生大鼠辣椒素处理的显著影响。