Koegler F H, Ritter S
Department of Veterinary Comparative Anatomy, Pharmacology and Physiology, College of Veterinary Medicine, Washington State University, Pullman 99164-6520, USA.
Obes Res. 1996 Jul;4(4):329-36. doi: 10.1002/j.1550-8528.1996.tb00240.x.
Galanin has been shown to stimulate feeding when injected intracranially in rats. Lesion and Fos studies have shown that the neural pathway for feeding stimulated by mercaptoacetate (MA)-induced blockade of fatty acid oxidation includes several structures rich in galanin cell bodies or terminals. In the present experiment, we examined the role of hindbrain galanin in feeding stimulated by MA. We found that galanin (1 nmol) stimulates feeding when injected in the nucleus of the solitary tract (NTS), a site that is crucial for MA-induced feeding, or into the fourth ventricle (4V, 1 or 5 nmol) and that NTS or 4V injections of the galanin receptor antagonist, M40 (1.5 or 5 nmol), completely blocked feeding induced by MA (68 mg/kg). The effect of the M40 appeared to be specific for MA-induced feeding, since M40 did not significantly attenuate either feeding induced by the antimetabolic glucose analog, 2-deoxy-D-glucose (2DG, 100 or 200 mg/kg), or deprivation-induced water intake. Results suggest that feeding induced by decreased fatty acid oxidation relies upon galaninergic terminals in the hindbrain. Furthermore, results indicate that hindbrain neurons involved in MA-induced feeding differ neurochemically from those important for 2DG-induced feeding.
在大鼠颅内注射时，甘丙肽已被证明能刺激进食。损伤和Fos研究表明，巯基乙酸（MA）诱导的脂肪酸氧化阻断所刺激的进食神经通路包括几个富含甘丙肽细胞体或终末的结构。在本实验中，我们研究了后脑甘丙肽在MA刺激进食中的作用。我们发现，当将甘丙肽（1 nmol）注射到孤束核（NTS，MA诱导进食的关键部位）或第四脑室（4V，1或5 nmol）时，它能刺激进食，并且向NTS或4V注射甘丙肽受体拮抗剂M40（1.5或5 nmol）可完全阻断MA（68 mg/kg）诱导的进食。M40的作用似乎对MA诱导的进食具有特异性，因为M40并未显著减弱抗代谢葡萄糖类似物2-脱氧-D-葡萄糖（2DG，100或200 mg/kg）诱导的进食或剥夺诱导的饮水。结果表明，脂肪酸氧化减少诱导的进食依赖于后脑的甘丙肽能终末。此外，结果表明，参与MA诱导进食的后脑神经元在神经化学上与对2DG诱导进食重要的神经元不同。
