Calingasan N Y, Ritter S
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, College of Veterinary Medicine, Washington State University, Pullman 99164-6520.
Am J Physiol. 1993 Nov;265(5 Pt 2):R1168-78. doi: 10.1152/ajpregu.1993.265.5.R1168.
Lesions of the area postrema/nucleus of the solitary tract (AP/NTS) region abolish feeding induced by mercaptoacetate (MA) and 2-deoxy-D-glucose (2DG), metabolic inhibitors that selectively impair fatty acid and glucose utilization, respectively. Because the AP/NTS region is important for both MA- and 2DG-induced feeding, the present experiment investigated the involvement of the lateral parabrachial nucleus (1PBN), which is innervated by AP/NTS neurons, in these feeding responses. Electrolytic and ibotenic acid lesions were directed at the entire parabrachial nucleus or at specific lateral parabrachial subnuclei. Rats with electrolytic lesions were tested for feeding in response to 0.9% NaCl (subcutaneous or intraperitoneal), MA (400, 600, and 800 mumol/kg ip), and 2DG (100 and 200 mg/kg sc). Ibotenate-lesioned rats were tested with NaCl and MA only. Lesions were verified either by cresyl violet staining or by glial fibrillary acidic protein immunohistochemistry. Bilateral destruction of the 1PBN severely impaired or abolished MA-induced feeding. Cell bodies important for MA-induced feeding appear to be localized in the dorsal-central 1PBN subnuclear area, because both electrolytic and cytotoxin microlesions centered in this area abolished feeding in response to MA. Fibers of passage important for MA-induced feeding appear to pass through the external and superior 1PBN because electrolytic but not cytotoxin lesions of these subnuclei disrupted the feeding response. In contrast, 2DG-induced feeding did not differ significantly from sham-lesioned controls in any of the 1PBN lesion groups. These results indicate that 2DG and MA stimulate feeding by activating separate central neural pathways and, perhaps, distinct metabolic controls of food intake.
最后区/孤束核（AP/NTS）区域的损伤消除了由巯基乙酸（MA）和2-脱氧-D-葡萄糖（2DG）诱导的进食，这两种代谢抑制剂分别选择性损害脂肪酸和葡萄糖的利用。由于AP/NTS区域对MA和2DG诱导的进食均很重要，本实验研究了受AP/NTS神经元支配的外侧臂旁核（lPBN）在这些进食反应中的作用。电解损伤和鹅膏蕈氨酸损伤针对整个臂旁核或特定的外侧臂旁亚核。对有电解损伤的大鼠进行测试，观察其对0.9%氯化钠（皮下或腹腔注射）、MA（400、600和800 μmol/kg腹腔注射）和2DG（100和200 mg/kg皮下注射）的进食反应。仅用氯化钠和MA对鹅膏蕈氨酸损伤的大鼠进行测试。通过甲酚紫染色或胶质纤维酸性蛋白免疫组织化学来证实损伤。双侧损毁lPBN严重损害或消除了MA诱导的进食。对MA诱导的进食重要的细胞体似乎定位于背中央lPBN亚核区域，因为以该区域为中心的电解损伤和细胞毒素微损伤均消除了对MA的进食反应。对MA诱导的进食重要的传导纤维似乎穿过外侧和上部lPBN，因为这些亚核的电解损伤而非细胞毒素损伤破坏了进食反应。相反，在任何lPBN损伤组中，2DG诱导的进食与假损伤对照组相比均无显著差异。这些结果表明，2DG和MA通过激活不同的中枢神经通路以及或许不同的食物摄入代谢控制来刺激进食。
