Grill H J, Friedman M I, Norgren R, Scalera G, Seeley R
Graduate Group of Psychology, University of Pennsylvania, Philadelphia 19104.
Am J Physiol. 1995 Mar;268(3 Pt 2):R676-82. doi: 10.1152/ajpregu.1995.268.3.R676.
Systemic injection of the fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) elicits a feeding response and induces c-fos activity in the parabrachial nuclei (PBN). We used bilateral ibotenic acid lesions of PBN to determine whether the activation inferred from c-fos activity was causally related to the feeding response. The relationship between the PBN lesion and feeding behavior was also examined with the glucose analogue 2-deoxy-D-glucose (2-DG). The PBN lesions interfered with the feeding response to 2,5-AM but spared the feeding response to 2-DG. Rats were also tested in a conditioned taste-aversion paradigm. Differences were observed in the relationship between lesion extent and behavioral deficit for feeding responses to 2,5-AM and taste-guided intake after taste-aversion conditioning. These data provide the first demonstration that central lesions can disrupt feeding responses to peripherally acting 2,5-AM. The results suggest that the neural substrate for this response differs from that mediating taste-aversion conditioning and from that involved in the feeding response to 2-DG.
全身性注射果糖类似物2,5-脱水-D-甘露醇（2,5-AM）会引发进食反应，并诱导臂旁核（PBN）中的c-fos活性。我们使用PBN的双侧鹅膏蕈氨酸损伤来确定从c-fos活性推断出的激活是否与进食反应存在因果关系。还使用葡萄糖类似物2-脱氧-D-葡萄糖（2-DG）研究了PBN损伤与进食行为之间的关系。PBN损伤干扰了对2,5-AM的进食反应，但未影响对2-DG的进食反应。大鼠还在条件性味觉厌恶范式中进行了测试。在损伤程度与对2,5-AM的进食反应以及味觉厌恶条件化后的味觉引导摄入量的行为缺陷之间的关系中观察到了差异。这些数据首次证明中枢损伤可破坏对外周作用的2,5-AM的进食反应。结果表明，这种反应的神经基质不同于介导味觉厌恶条件化的神经基质，也不同于参与对2-DG进食反应的神经基质。
