6533b827fe1ef96bd12867e6
RESEARCH PRODUCT
Selective erasure of a fear memory
Paul W. FranklandRachael L. NeveAri WaismanAdelaide P. YiuSteven A. KushnerJin-hee HanSheena A. JosselynHwa-lin Liz HsiangBruno BontempiThorsten Buchsubject
AmnesiaApoptosisMice TransgenicCREBAmygdalaMice03 medical and health sciences0302 clinical medicineMemoryConditioning PsychologicalmedicineAnimalsMemory disorderCyclic AMP Response Element-Binding ProteinNeuronal memory allocation030304 developmental biologyMemory consolidation0303 health sciencesMultidisciplinarybiologyCREBMemoriaFearmedicine.diseaseAmygdalamedicine.anatomical_structurenervous systemMental Recallbiology.proteinMemory traceMemory consolidation[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]AmnesiaNeuronPavlovian conditioningmedicine.symptomNeuroscience030217 neurology & neurosurgerydescription
International audience; 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.
year | journal | country | edition | language |
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2009-03-13 | Science |