1994 BIO Minority Postdoctoral Research Fellowship

这一行动满足了NSF少数民族博士后研究奖学金。这些研究探讨了阿片受体在海马苔藓纤维- ca3突触长期增强（LTP）过程中诱导晚期基因的作用。LTP是一种相对持久的突触效率增加，由传入纤维的短暂、高频刺激引起，被广泛认为是哺乳动物学习和记忆的候选机制。海马苔藓纤维- ca - 3突触的LTP依赖于阿片受体的激活，需要蛋白质合成和基因表达。据推测，迟动基因在LTP的维持和学习记忆中起重要作用。本研究通过确定阿片类拮抗剂和肽激动剂的作用，通过破坏海马晚期基因的翻译，通过检查晚期基因被破坏的动物，以及确定学习和记忆任务表现的变化，直接验证了这一假设。新的基因表达在突触可塑性和更高的生理过程中的作用将被确定。

This action fulds an NSF Minority Postdoctoral Research Fellowship. These studies examine the role of opioid receptors in the induction of late genes during long-term potentiation (LTP) at the hippocampal mossy fiber-CA3 synapse. LTP is a relatively long-lasting increase in synaptic efficiency resulting from brief, high frequency stimulation of afferent fibers and is widely accepted as a candidate mechanism for learning and memory in mammals. LTP at the mossy fiber-CA 3 synapse of the hippocampus depends on the activation of opioid receptors, requiring protein synthesis and gene expression. It is hypothesized that late acting genes play important roles in maintenance of LTP and in learning and memory. This research directly tests this hypothesis by determining the effects of opioid antagonists and peptide agonists, by disrupting translation of hippocampal late genes, by examining animals with disrupted late genes, and determining changes in performance in learning and memory tasks. The role of new gene expression in synaptic plasticity and in higher physiological processes will be determined.