BRAIN-STEM SYSTEMS MEDIATE THE ENHANCEMENT OF PALATABILITY BY CHLORDIAZEPOXIDE
BRAIN-STEM SYSTEMS MEDIATE THE ENHANCEMENT OF PALATABILITY BY CHLORDIAZEPOXIDE
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DOI：
10.1016/0006-8993(88)91128-6
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发表时间：
1988-05-03
期刊：
影响因子：
2.9
通讯作者：
BERRIDGE, KC
中科院分区：
文献类型：
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作者：
BERRIDGE, KC
先前的研究表明，苯二氮卓受体复合物参与利眠宁（CDP）给药后味觉适口性的增强。 CDP (10 mg/kg) 可促进大鼠经口输注味道引起的积极的、适口性依赖性的摄入反应，并且这种作用可被苯二氮卓类拮抗剂逆转。相比之下，CDP 不会促进大鼠更中性或厌恶的反应。由于前脑中苯二氮卓类受体的密度最高，因此将前脑结构作为 CDP 作用的场所似乎是合理的。然而，苯二氮卓类受体确实存在于尾部脑干中（尽管密度较低），并且分离的去大脑脑干已被证明具有相当大的味觉处理和反应能力。本研究检查了 CDP 对慢性中脑去大脑大鼠味觉反应性的影响。结果表明，即使在与前脑没有通讯的情况下，CDP 也可以作用于间脑下脑干，增强积极的摄入反应。这表明相关的苯二氮卓受体和调节味觉反应所需的最小神经回路都存在于中脑内部或下方。
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.