BEHAVIORAL SENSITIZATION

这个项目的总体目标是研究现象学， 以及行为感觉的生化和神经解剖学基础， zation.该模型用于研究行为病理学的演变 以及条件作用或情境依赖在这些行为中的作用。 环境和药物干预措施进行了调查， 试图改变敏感化发展和表达的过程。 迄今为止的重大发现包括以下方面的证明： 一种新的两天可卡因致敏范式，这是上下文依赖的， nt; 2）第二致敏范例，使用三天预处理 方案，这也是依赖于上下文，是更持久的比 上述范例; 3）完整的多巴胺功能的要求， 发展而不是表达依赖于情境的敏感性; 4)杏仁核和脑桥核在这种致敏中的作用; 5)可卡因和NMDA拮抗剂MK-801之间的交叉致敏， 可卡因和普鲁卡因（一种自我管理的局部麻醉剂， 但可卡因和利多卡因（利多卡因不是 自我管理）或可卡因和咖啡因。

The overall objectives of this project are to study the phenomenology, and the biochemical and neuroanatomical substrates of behavioral sensiti- zation. This model is used to study the evolution of behavioral pathology and the role of conditioning or context-dependency in such behaviors. Environmental and pharmacological interventions are investigated in an attempt to alter the course of sensitization development and expression. Significant findings to date include demonstration of the following: 1) a novel two day cocaine sensitization paradigm which is context-depende- nt; 2) a second sensitization paradigm, using a three day pretreatment regimen, which is also context-dependent and is more long-lasting than the above paradigm; 3) the requirement of intact dopamine function for the development, but not expression of context-dependent sensitization; 4) a role for the amygdala and nucleus accumbens in this sensitization; 5) cross sensitization between cocaine and the NMDA antagonist MK-801, and between cocaine and procaine ( a local anesthetic that is self-admin- istered by primates), but not between cocaine and lidocaine (which is not self-administered) or cocaine and caffeine.