BEHAVIORAL SENSITIZATION

这个项目的总体目标是研究现象学， 以及行为的生化和神经解剖学基础 敏化。该模型被用来研究行为的演化。 病理学以及条件反射或语境依赖在这一过程中的作用 行为。环境和药物干预措施包括 调查的目的是试图改变敏感化的过程 发展与表达。到目前为止的重要发现包括 论证如下：1)一种新型的两天可卡因敏化 依赖于上下文的范例；2)第二敏化范例， 使用三天的预处理方案，这也是依赖于上下文的 而且比上述范式更持久；3) 完整的多巴胺功能参与发育，但不表达 上下文相关的敏感化；4)杏仁核和核团的作用 5)可卡因之间的交叉增敏作用 和NMDA拮抗剂MK-801，以及可卡因和普鲁卡因之间(a 局麻药，由灵长类自行给药)，但不是在 可卡因和利多卡因(非自行给药)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 sensitization. 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-dependent; 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 importance 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-administered by primates), but not between cocaine and lidocaine (which is not self-administered) or cocaine and caffeine.