Morley B J, Garner L L
Research Division, Boys Town National Institute for Communication Disorders in Children, Omaha, NE 68131.
Brain Res. 1990 Jun 11;519(1-2):1-5. doi: 10.1016/0006-8993(90)90053-e.
Sodium-dependent, high-affinity choline uptake (HACU) and the density of alpha-bungarotoxin (BuTX) receptor-binding sites were measured in the hippocampus following the intraventricular infusion of ethylcholine aziridinium ion (AF64A), a neurotoxin that competes with choline at high-affinity choline transport sites and may result in the degeneration of cholinergic axons. Eight days after the infusion of AF64A into the lateral ventricles (2.5 nmol/side), HACU was depleted by 60% in the hippocampus of experimental animals in comparison with controls, but the density of BuTX-binding sites was not altered. The administration of 15 mg/ml of choline chloride in the drinking water increased the density of BuTX-binding sites, as previously reported by this laboratory. The administration of AF64A did not prevent the effect of exogenous choline on the density of binding sites, nor did choline treatment alter the effect of AF64A on HACU. These data indicate that the density of BuTX-binding sites in the hippocampus is not altered following a substantial decrease in HACU and presumed degeneration of cholinergic axons. Since the effect of exogenous choline was not prevented by AF64A treatment, the data are interpreted to support the hypothesis that the increase in the density of BuTX-binding sites following dietary choline supplementation is attributable to a direct effect of choline on receptor sites.
在脑室内注入氮丙啶离子乙基胆碱（AF64A）后，测定海马体中钠依赖性高亲和力胆碱摄取（HACU）和α-银环蛇毒素（BuTX）受体结合位点的密度。AF64A是一种神经毒素，在高亲和力胆碱转运位点与胆碱竞争，可能导致胆碱能轴突退化。向侧脑室注入AF64A（2.5 nmol/侧）八天后，与对照组相比，实验动物海马体中的HACU减少了60%，但BuTX结合位点的密度没有改变。如本实验室先前报道，在饮用水中给予15 mg/ml的氯化胆碱可增加BuTX结合位点的密度。给予AF64A并未阻止外源性胆碱对结合位点密度的影响，胆碱处理也未改变AF64A对HACU的影响。这些数据表明，在HACU大幅下降及推测胆碱能轴突退化后，海马体中BuTX结合位点的密度并未改变。由于AF64A处理并未阻止外源性胆碱的作用，这些数据被解释为支持以下假设：饮食中补充胆碱后BuTX结合位点密度的增加归因于胆碱对受体位点的直接作用。
