Journal
SCIENCE
Volume 323, Issue 5920, Pages 1492-1496Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1164139
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Funding
- Canadian Institutes of Health Research [MOP74650, MOP77561]
- EJLB Foundation
- National Alliance for Research on Schizophrenia and Depression [fellowship]
- France-Canada Research Foundation [travel fellowship]
- Agence Nationale de la Recherche (France) [06-NEURO-027-03]
- Hospital for Sick Children [Restracomp Fellowships]
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Memories are thought to be encoded by sparsely distributed groups of neurons. However, identifying the precise neurons supporting a given memory (the memory trace) has been a long-standing challenge. We have shown previously that lateral amygdala (LA) neurons with increased cyclic adenosine monophosphate response element-binding protein (CREB) are preferentially activated by fear memory expression, which suggests that they are selectively recruited into the memory trace. We used an inducible diphtheria-toxin strategy to specifically ablate these neurons. Selectively deleting neurons overexpressing CREB (but not a similar portion of random LA neurons) after learning blocked expression of that fear memory. The resulting memory loss was robust and persistent, which suggests that the memory was permanently erased. These results establish a causal link between a specific neuronal subpopulation and memory expression, thereby identifying critical neurons within the memory trace.
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