ANATOMY AND PHARMACOLOGY OF FEAR-POTENTIATED STARTLE

联想的神经解剖学和神经化学机制 学习，使用大鼠的声学惊吓反射，将是 调查过了。声学惊吓是一种短潜伏期反射，由 简单的神经通路。惊吓幅度可以通过引出来增加 在先前与电击配对的光线存在时的反射 (恐惧强化或恐惧强化的惊吓)。这种效果可以被阻断。 通过临床上减轻焦虑的药物，通过中枢损害 杏仁核或损害，阻止视觉信息 到达杏仁核。杏仁核的低水平电刺激 通过直接投影显著增加声学惊吓幅度 从杏仁核到声学惊吓回路。因此， 恐惧强化的惊吓是动物恐惧或焦虑的一种模型。 其中大部分神经回路已经被勾画出来。因此，现在是 有可能开始确定两者所涉及的细胞机制 联想恐惧条件反射的习得和表达。 兴奋性氨基酸受体在习得中的作用， 恐惧强化的惊吓的表达和消退将通过 局部输注N-甲基-D-天冬氨酸(NMDA)与非NMDA受体的比较 在恐惧增强之前，拮抗剂进入不同的杏仁核 使用视觉惊吓训练、测试或消亡会议 有条件的。蛋白激酶抑制剂的可能作用也将是 已评估。其他研究将测试NMDA拮抗剂是否会赢得阻止 在培训结束后立即给予的收购。其他研究将 评估NMDA拮抗剂是否会影响获得性与表达 使用听觉条件性刺激或 上下文线索。其他研究赢得了地方政府的测试效果 进入声学惊吓通路，开始测试细胞 关于杏仁核如何通过激活而增加惊吓的假说 它直接投射到惊吓环路。结果将会有 对理解学习和记忆的神经基础的启示， 以及更具体的抗焦虑药物的潜在开发。

Neuroanatomical and neurochemical mechanisms involved in associative learning, using the acoustic startle reflex in rats, will be investigated. Acoustic startle is a short latency reflex mediated by a simple neural pathway. Startle amplitude can be increased by eliciting the reflex in the presence of a light previously paired with a shock (fear-enhanced or fear-potentiated startle). This effect can be blocked by drugs which reduce anxiety clinically, by lesions of the central nucleus of the amygdala or lesions that prevent visual information from reaching the amygdala. Low level electrical stimulation of the amygdala markedly increases acoustic startle amplitude via a direct projection from the amygdala to the acoustic startle circuit. Thus, fear-potentiated startle represents a model of fear or anxiety in animals where much of the neural circuitry has been delineated. Hence, it is now possible to begin to determine the cellular mechanisms involved in both the acquisition and expression of associative fear conditioning. The role of excitatory amino acid receptors in acquisition, expression and extinction of fear-potentiated startle will be analyzed by locally infusing N-methyl-D-aspartate (NMDA) vs. nonNMDA receptor antagonists into different amygdala nuclei before fear-potentiated startle training,testing or extinction sessions using a visual conditioned. Possible roles of protein kinase inhibitors will also be evaluated. Other studies will test if NMDA antagonists win block acquisition when given immediately after training. Other studies will evaluate whether NMDA antagonists will affect acquisition vs. expression of potentiated startle using either an auditory conditioned stimulus or contextual cues. Other studies win test effects of local administration of drugs into the acoustic startle pathway to begin to test cellular hypotheses about how activation of the amygdala can increase startle via its direct projection to the startle circuit. The results will have implications for understanding the neural basis of learning and memory, as well as potential development of more specific anxiolytic drugs.