A study published in Nature (484(7394): 381–385. doi:10.1038/nature11028) demonstrates that optogenetic stimulation of hippocampal neurons activated during fear conditioning can induce fear memory recall. The researchers used channelrhodopsin-2 (ChR2) to label neurons in the dentate gyrus (DG) of the hippocampus that were active during fear learning. These neurons were then optically reactivated in a different context, leading to increased freezing behavior, a sign of fear memory recall. This effect was not observed in mice without fear conditioning or in those with different cell labeling, indicating that the memory recall was context-specific. The study shows that a sparse population of hippocampal neurons, which are active during learning, is sufficient for memory recall when reactivated. The findings suggest that these neurons form a memory engram, a cellular basis for memory storage. The study also highlights the importance of the DG in contextual memory formation and the role of optogenetic techniques in mapping memory-related neural circuits. The results indicate that activating a specific subset of neurons involved in memory formation can elicit the behavioral expression of that memory, supporting the idea that memory is encoded by a sparse population of neurons. The study provides a general method for mapping cellular populations associated with memory engrams. The research also addresses the necessity of these sparse cell populations in memory processes, as shown by previous studies. The findings contribute to understanding how memories are formed and stored in the brain, and how they can be retrieved through specific neural activation. The study's methods involve virus-mediated gene expression, immunohistochemistry, in vivo recording, and behavioral tests to examine the effects of optogenetic stimulation on memory recall. The results demonstrate that optogenetic activation of DG neurons can induce fear memory recall, providing insights into the neural mechanisms underlying memory formation and retrieval.A study published in Nature (484(7394): 381–385. doi:10.1038/nature11028) demonstrates that optogenetic stimulation of hippocampal neurons activated during fear conditioning can induce fear memory recall. The researchers used channelrhodopsin-2 (ChR2) to label neurons in the dentate gyrus (DG) of the hippocampus that were active during fear learning. These neurons were then optically reactivated in a different context, leading to increased freezing behavior, a sign of fear memory recall. This effect was not observed in mice without fear conditioning or in those with different cell labeling, indicating that the memory recall was context-specific. The study shows that a sparse population of hippocampal neurons, which are active during learning, is sufficient for memory recall when reactivated. The findings suggest that these neurons form a memory engram, a cellular basis for memory storage. The study also highlights the importance of the DG in contextual memory formation and the role of optogenetic techniques in mapping memory-related neural circuits. The results indicate that activating a specific subset of neurons involved in memory formation can elicit the behavioral expression of that memory, supporting the idea that memory is encoded by a sparse population of neurons. The study provides a general method for mapping cellular populations associated with memory engrams. The research also addresses the necessity of these sparse cell populations in memory processes, as shown by previous studies. The findings contribute to understanding how memories are formed and stored in the brain, and how they can be retrieved through specific neural activation. The study's methods involve virus-mediated gene expression, immunohistochemistry, in vivo recording, and behavioral tests to examine the effects of optogenetic stimulation on memory recall. The results demonstrate that optogenetic activation of DG neurons can induce fear memory recall, providing insights into the neural mechanisms underlying memory formation and retrieval.