Mercer J G, Lawrence C B, Morgan P J
Rowett Research Institute, Bucksburn, Aberdeen, UK.
Physiol Behav. 1993 Jun;53(6):1061-5. doi: 10.1016/0031-9384(93)90360-r.
The ability of nanomolar concentrations of guanine, but not adenine, nucleotides to inhibit specific 125I-Bolton-Hunter CCK binding to ligated rat vagus nerve demonstrated that vagal CCK binding sites were linked to G-proteins during axonal transport. The GTP analogue, GTP[S], reduced specific binding to both anterogradely and retrogradely transported binding sites by more than 90% at 1 microM. Transport of these putative receptor-G-protein complexes was examined under conditions of food deprivation or physiological hyperphagia induced by either lactation or genetic obesity. None of the physiological or imposed manipulations of food intake had any effect on the axonal transport of CCK binding sites. Transection of the cervical vagus resulted in an accumulation of binding sites at the lesion site that was indistinguishable from that seen following ligation for the same period.
纳摩尔浓度的鸟嘌呤核苷酸(而非腺嘌呤核苷酸)抑制特异性125I-博尔顿-亨特胆囊收缩素(CCK)与结扎大鼠迷走神经的结合,这表明迷走神经CCK结合位点在轴突运输过程中与G蛋白相连。GTP类似物GTP[S]在1微摩尔浓度时,使顺行和逆行运输的结合位点的特异性结合减少了90%以上。在食物剥夺或由哺乳或遗传性肥胖引起的生理性多食条件下,研究了这些假定的受体-G蛋白复合物的运输。食物摄入的任何生理或人为操作对CCK结合位点的轴突运输均无影响。颈迷走神经横断导致损伤部位结合位点的积累,这与同期结扎后所见的情况无明显差异。