Stein E A, Carr K D, Simon E J
Department of Psychiatry, Medical College of Wisconsin, Milwaukee 53226.
Brain Res. 1990 Nov 19;533(2):213-22. doi: 10.1016/0006-8993(90)91342-e.
Although opioid antagonists block feeding behavior in a variety of animal models, the number and identity of CNS regions in which the inferred endogenous opioid activity mediates feeding have yet to be established. Furthermore, it is not yet clear whether the opioid activity that sustains feeding is a concomitant of the appetitive motivational state or the consummatory response. In an effort to address these issues, an in vivo autoradiographic method was used to visualize CNS regional changes in opioid release during appetitively motivating electrical stimulation in the lateral hypothalamus (ESLH) and during consummatory behavior elicited by such stimulation. Regional decreases in [3H]diprenorphine [(3H]Dpr) binding, suggesting increased release of an endogenous opioid peptide, were observed in the medial prefrontal cortex, medial septum, gustatory cortex, zona incerta, mediodorsal thalamus, and hippocampus of rats receiving ESLH. Decreased binding in the latter 4 structures did not appear when animals were allowed to eat during ESLH, suggesting that the inferred opioid release is associated with appetitive behaviors elicited by ESLH which are suppressed when food is available and consummatory behavior predominates. When animals were allowed to eat during ESLH, [3H]Dpr binding in anterior cingulate cortex decreased substantially, suggesting that feeding behavior specifically triggers opioid release in this region. ESLH and feeding were found to increase [3H]Dpr binding in a number of CNS regions. Alternative explanations for increased binding, including inhibition of tonic opioid release, changes in cerebral blood flow, and opioid receptor up-regulation are discussed.
尽管阿片类拮抗剂在多种动物模型中均可阻断进食行为，但内源性阿片活性介导进食的中枢神经系统（CNS）区域的数量和具体部位尚未明确。此外，维持进食的阿片活性是与食欲动机状态还是与进食反应相伴，目前也尚不清楚。为了解决这些问题，我们采用了一种体内放射自显影方法，以观察在外侧下丘脑进行诱发食欲的电刺激（ESLH）期间及由此刺激引发的进食行为期间，CNS区域阿片释放的变化。在接受ESLH的大鼠的内侧前额叶皮质、内侧隔区、味觉皮质、未定带、背内侧丘脑和海马中，观察到[3H]二丙诺啡[（3H）Dpr]结合减少，提示内源性阿片肽释放增加。当动物在ESLH期间进食时，后4种结构中的结合并未减少，这表明推测的阿片释放与ESLH引发的食欲行为有关，当有食物且进食行为占主导时，这种食欲行为会受到抑制。当动物在ESLH期间进食时，前扣带回皮质中的[3H]Dpr结合大幅减少，这表明进食行为会特异性地触发该区域的阿片释放。研究发现，ESLH和进食会增加多个CNS区域的[3H]Dpr结合。文中还讨论了结合增加的其他解释，包括对阿片持续释放的抑制、脑血流量的变化以及阿片受体上调。
