Moran T H, Smith G P, Hostetler A M, McHugh P R
Brain Res. 1987 Jul 7;415(1):149-52. doi: 10.1016/0006-8993(87)90278-2.
In order to evaluate vagal cholecystokinin (CCK) binding sites as potential target sites for the satiety actions of CCK, their presence, axonal flow and pharmacological specificity in subdiaphragmatic vagal branches were examined by autoradiography utilizing 125I-Bolton Hunter CCK-33. Specific CCK binding and axonal transport were found in vagal trunks and all abdominal vagal branches. Binding was inhibited by unlabelled CCK-8, but not by desulfated CCK-8. The pharmacological specificity and transport of CCK binding sites to subdiaphragmatic branches indicate a potential role in mediating CCK's satiety effect.
为了评估迷走神经胆囊收缩素（CCK）结合位点作为CCK饱腹感作用的潜在靶点，利用125I-博尔顿·亨特CCK-33通过放射自显影术检查了膈下迷走神经分支中这些结合位点的存在、轴浆运输和药理学特异性。在迷走神经干和所有腹部迷走神经分支中发现了特异性CCK结合和轴突运输。未标记的CCK-8可抑制结合，但去硫酸化CCK-8则不能。CCK结合位点对膈下分支的药理学特异性和运输表明其在介导CCK饱腹感效应中具有潜在作用。
