The neural circuit basis of infantile amnesia

点击翻译按钮获取中文摘要

The overall goal of my research program is to understand how the brain stores and processes information. This program is composed of two non-overlapping components. The first component is concerned with how information processing is altered in disease states, and is supported by CIHR. The second component is concerned with understanding the basic mechanistic biology of information processing, and is supported by NSERC. NSERC has continuously supported my lab's work on these basic and fundamental brain processes since 2005. The current renewal-focused on developmental aspects of memory-has no conceptual or budgetary overlap with our health-related CIHR-funded work. Why do we forget our earliest memories? This phenomenon-termed infantile amnesia-has been characterized extensively by psychologists, and a universal pattern has emerged. As adults, we can remember many events from our childhood. However, we remember hardly any events from the first 3-4 years of our lives. Psychological theories of infantile amnesia emphasize the co-emergence of things like language, self-identity and theory of mind with the emerging ability to form lasting memories for important events in our lives. However, non-human mammals also exhibit accelerated forgetting in infancy indicating that it is unlikely that this phenomenon can be entirely explained using human-specific concepts. Instead, others have argued that protracted brain development may interfere with the ability to stably encode and store memories for events. The goal of my NSERC renewal is to identify features of protracted brain development are responsible for infantile amnesia. The medial prefrontal cortex (mPFC) plays an important role in the encoding and consolidation of event memories, and the long-range connectivity of mPFC evolves across development. Here, we will test the specific hypothesis that the emergence of late-forming projections (e.g., mPFC--> basolateral amygdala) are causally related to the ability to form enduring memories for events. We will characterize structural and functional connectivity of mPFC long-range connections across development, and ask whether optogenetically disabling these connections in older mice regresses them back to a younger state where event memories are rapidly forgotten. We will further ask whether sex and species differences in infantile amnesia are also causally related to differential maturation rates of these late-forming mPFC long-range connections. My lab provides an excellent environment for training HQP. I develop individualized mentorship plans for each trainee that emphasize technical and communication skills and career development. In the past 6 yeas, trainees have contributed to 63 publications, and have moved on to academic and non-academic positions. Equity, diversity and inclusivity is central to my lab training philosophy, and I am proud that demographics within my lab reflect those in the immediate outside world (i.e., Toronto).