Lateral parabrachial lesions attenuate ingestive effects of area postrema lesions.
Lateral parabrachial lesions attenuate ingestive effects of area postrema lesions.
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外侧臂旁病变减弱了后区病变的摄取作用。
DOI：
10.1152/ajpregu.1989.256.2.r306
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Ritter,RC
中科院分区：
文献类型：
--
作者：
Edwards,GL;Ritter,RC
孤束核最后区和邻近核的病变（AP病变）导致大鼠在短期试验中消耗增加的可口食物量。由于外侧臂旁核（IPBN）接受来自AP和孤束邻近核的突出的传入投射，因此IPBN可能在AP损伤大鼠中观察到的摄食行为改变中起作用。本研究探讨的作用，lPBN在过度摄入的高度可口的食物后，AP病变。我们发现，单独的lPBN损伤不会导致大鼠消耗更多的可口食物。相反，当在AP病变之前产生IPBN病变时，没有发生高可口食物的摄入增加。此外，当AP损伤的大鼠接受随后的lPBN病变，以前建立的美味食物的过度摄入被废除。这些结果表明，lPBN是必要的AP病变引起的过度摄取高可口的食物的发病机制。
Lesions of the area postrema and adjacent nucleus of the solitary tract (AP lesions) cause rats to consume increased amounts of palatable food in short duration tests. Because the lateral parabrachial nucleus (lPBN) receives a prominent afferent projection from the AP and adjacent nucleus of the solitary tract, it is possible the lPBN plays a role in the altered ingestive behaviors observed in AP-lesioned rats. The present study examines the role of the lPBN in overingestion of highly palatable foods subsequent to AP lesions. We found that lesions of the lPBN alone did not cause rats to consume increased amounts of palatable food. Rather, when lPBN lesions were produced before AP lesions, increased intake of highly palatable food did not occur. Moreover, when AP-lesioned rats received subsequent lPBN lesions, the previously established overingestion of palatable foods was abolished. These results indicate that the lPBN is necessary in the pathogenesis of AP lesion-induced overingestion of highly palatable foods.