PARAVENTRICULAR NUCLEUS LESIONS ABOLISH THE INHIBITION OF FEEDING INDUCED BY SYSTEMIC CHOLECYSTOKININ
PARAVENTRICULAR NUCLEUS LESIONS ABOLISH THE INHIBITION OF FEEDING INDUCED BY SYSTEMIC CHOLECYSTOKININ
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DOI：
10.1016/0196-9781(85)90324-9
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发表时间：
1985-01-01
期刊：
影响因子：
3
通讯作者：
KISS, JZ
中科院分区：
文献类型：
--
作者：
CRAWLEY, JN;KISS, JZ
外周给药胆囊收缩素（CCK）引发一种行为综合征，包括减少食物消耗和减少探索行为。先前的研究表明，CCK刺激肠道内的受体，激活迷走神经，将感觉信息传递给孤束核（NTS）及其上行通路[5,6,7,41]。NTS上行投射的末端区域包括下丘脑室旁核（PVN）、杏仁核中央核（CNA）和纹状末端床核（BNST）。在大鼠身上对这三个靶点进行损伤，以验证突触后结构介导CCK诱导的行为综合征的假设。PVN的刀切损伤消除了CCK（5和10 .mu）引起的摄食减少。g/kg IP)，与假性损伤对照大鼠相比。PVN病变仅部分减弱CCK（2.5、5和10 .mu）引起的探查减少。g/kd IP)，与假性损伤对照大鼠相比。CNA的电解损伤部分减弱了CCK（2.5、5和10 .mu）引起的探索行为的减少。g/kg IP)，对CCK（5和10 .mu）诱导的采食量减少没有影响。克/公斤IP)。BNST的电解损伤对CCK引起的进食减少和探索减少都没有影响。PVN似乎是调节CCK对摄食行为的一个关键的前脑靶点。CNA似乎促进了CCK在勘探方面的行动。CCK引起的行为综合征的各个组成部分可能由解剖学上不同的前脑位点介导。
Peripherally administered cholecystokinin (CCK) initiates a behavioral syndrome which includes reduced food consumption and reduced exploratory behaviors. Previous studies suggest that CCK stimulates receptors in the gut, activating the vagus nerve, which relays sensory information to the nucleus tractus solitarius (NTS) and its ascending pathways [5, 6, 7, 41]. Terminal regions of ascending NTS projections include the paraventricular nucleus of the hypothalamus (PVN), the central nucleus of the amygdala (CNA), and the bed nucleus of the stria terminals (BNST). Lesions of these three target sites were performed in rats to test the hypothesis that structures postsynaptic to the NTS mediate the behavioral syndrome induced by CCK. Knife cut lessions of the PVN abolished the reductions in feeding induced by CCK (5 and 10 .mu.g/kg IP), as compared to sham lesioned control rats. PVN lesions only partially attenuated the reductions in exploration induced by CCK (2.5, 5, and 10 .mu.g/kd IP), as compared to sham lesioned control rats. Electrolytic lesions of the CNA partially attenuated the reductions in exploratory behavior induced by CCK (2.5, 5, and 10 .mu.g/kg IP), and had no effect on the reductions in feeding induced by CCK (5 and 10 .mu.g/kg IP). Electrolytic lesions of the BNST had no effect on either the reductions in feeding or the reductions in exploration induced by CCK. The PVN appears to be one critical forebrain target site for mediating the actions of CCK on feeding. The CNA appears to facilitate the actions of CCK on exploration. Individual components of the behavioral syndrome induced by CCK may be mediated by anatomically distinct forebrain loci.