Ladenheim E E, Ritter R C
Department of Veterinary and Comparative Anatomy, Washington State University, Pullman 99164.
Am J Physiol. 1991 Feb;260(2 Pt 2):R263-6. doi: 10.1152/ajpregu.1991.260.2.R263.
This study was conducted to evaluate the extent to which bombesin (BBS)-induced suppression of food intake relies on small, unmyelinated sensory neurons. Rats were pretreated intraperitoneally with capsaicin, a neurotoxin that destroys a subpopulation of small-diameter sensory neurons, and tested for suppression of food intake after intraperitoneal administration of 2, 4, 8, 16, and 32 micrograms/kg BBS. Capsaicin pretreatment attenuated suppression of food intake by BBS over a wide range of doses. The site of capsaicin action was not determined in this study. However, work by others indicates that vagal and nonvagal neural substrates participate in suppression of food intake by BBS. Afferents of both of these substrates are predominantly small and unmyelinated. Therefore, the deficits in BBS-induced suppression of food intake that we observed may reflect damage to both vagal and/or nonvagal neurons that participate in BBS-induced suppression of food intake.
本研究旨在评估蛙皮素（BBS）诱导的食物摄入量抑制在多大程度上依赖于细小的无髓鞘感觉神经元。给大鼠腹腔注射辣椒素（一种可破坏小直径感觉神经元亚群的神经毒素）进行预处理，然后在腹腔注射2、4、8、16和32微克/千克BBS后测试食物摄入量的抑制情况。辣椒素预处理在很宽的剂量范围内减弱了BBS对食物摄入量的抑制作用。本研究未确定辣椒素的作用部位。然而，其他人的研究表明，迷走神经和非迷走神经底物参与了BBS对食物摄入量的抑制。这两种底物的传入神经主要是细小的无髓鞘神经。因此，我们观察到的BBS诱导的食物摄入量抑制缺陷可能反映了参与BBS诱导的食物摄入量抑制的迷走神经和/或非迷走神经神经元的损伤。
