Berridge K C
Department of Psychology, University of Michigan, Ann Arbor 48109.
Brain Res. 1988 May 3;447(2):262-8. doi: 10.1016/0006-8993(88)91128-6.
Previous studies have indicated that the benzodiazepine receptor complex is involved in enhancing taste palatability after chlordiazepoxide (CDP) administration. Positive, palatability-dependent ingestive reactions elicited by orally infused tastes are facilitated in rats by CDP (10 mg/kg), and this effect is reversible by benzodiazepine antagonists. In contrast, the rats' more neutral or aversive reactions are not facilitated by CDP. Because benzodiazepine receptors exist in highest density in the forebrain, it has seemed plausible to posit forebrain structures as the locus of CDP action. However, benzodiazepine receptors do exist in the caudal brainstem (albeit in lesser density), and the isolated decerebrate brainstem has been demonstrated to possess considerable taste processing and response capacity. The present study examined the effects of CDP on taste reactivity in chronic mesencephalic decerebrate rats. The results show that CDP can act on the subdiencephalic brainstem to enhance positive ingestive reactions even in the absence of communications with the forebrain. This indicates that both the relevant benzodiazepine receptors and the minimal neural circuit needed to modulate taste reactivity exist within or below the mesencephalon.
先前的研究表明，苯二氮䓬受体复合物在给予氯氮卓（CDP）后参与增强味觉适口性。口服注入味道引发的积极的、适口性依赖的摄食反应在大鼠中会被CDP（10毫克/千克）促进，并且这种效应可被苯二氮䓬拮抗剂逆转。相比之下，大鼠更中性或厌恶的反应不会被CDP促进。由于苯二氮䓬受体在前脑中密度最高，因此将前脑结构假定为CDP作用位点似乎是合理的。然而，苯二氮䓬受体确实存在于脑桥尾端（尽管密度较低），并且已证明离体的去大脑脑干具有相当大的味觉处理和反应能力。本研究检测了CDP对慢性中脑去大脑大鼠味觉反应性的影响。结果表明，即使在与前脑没有联系的情况下，CDP也可作用于间脑下脑干以增强积极的摄食反应。这表明相关的苯二氮䓬受体以及调节味觉反应性所需的最小神经回路存在于中脑内或中脑以下。
