Our past experiences shape our current and future behavior. These experiences must leave some enduring imprint on our brains, altering neural circuits that mediate behavior and contributing to our individual differences. As a framework for understanding how experiences might produce lasting changes in neural circuits, Clayton [D. F. Clayton, Neurobiol. Learn. Mem. 74, 185–216 (2000)] introduced the concept of the genomic action potential (gAP)—a structured genomic response in the brain to acute experience. Similar to the familiar electrophysiological action potential (eAP), the gAP also provides a means for integrating afferent patterns of activity but on a slower timescale and with longer-lasting effects. We revisit this concept in light of contemporary work on experience-dependent modification of neural circuits. We review the “Immediate Early Gene” (IEG) response, the starting point for understanding the gAP. We discuss evidence for its involvement in the encoding of experience to long-term memory across time and biological levels of organization ranging from individual cells to cell ensembles and whole organisms. We explore distinctions between memory encoding and homeostatic functions and consider the potential for perpetuation of the imprint of experience through epigenetic mechanisms. We describe a specific example of a gAP in humans linked to individual differences in the response to stress. Finally, we identify key objectives and new tools for continuing research in this area.

我们过去的经验影响着我们当前和未来的行为。这些经历必须在我们的大脑上留下持久的印记，改变介导行为并导致我们个体差异的神经回路。作为了解经验如何在神经回路中产生持久变化的框架，Clayton [DF Clayton，Neurobiol。学。嗯[74，185–216（2000）]提出了基因组动作电位（gAP）的概念，即大脑对急性经历的结构化基因组反应。与熟悉的电生理动作电位（eAP）相似，gAP还提供了一种整合传入活动模式的方法，但时间尺度较慢且效果更持久。我们根据有关神经回路的经验依赖型修改的当代工作来重新审视这个概念。我们回顾了“立即早期基因”（IEG）反应，这是了解gAP的起点。我们讨论了其参与跨时间和长期的经验编码以及组织的生物学水平（从单个细胞到细胞团和整个生物体）的证据。我们探索记忆编码和体内平衡功能之间的区别，并考虑通过表观遗传机制永久保留经验的烙印。我们描述了人类中gAP的一个特定示例，该gAP与对压力的反应中的个体差异有关。最后，我们确定了关键目标和新工具，可以继续在这一领域进行研究。