Journal
NEURON
Volume 107, Issue 2, Pages 283-+Publisher
CELL PRESS
DOI: 10.1016/j.neuron.2020.04.013
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Funding
- Leon Levy Foundation
- American Psychiatric Foundation
- NIH [T32MH018870, K08MH113036, T32NS064928, F31MH121058, K25DC013557, R01MH100631, U19NS090583, R01NS094668]
- National Science Foundation (NSF) NeuroNex program [DBI-1707398]
- Simons Charitable Foundation
- Grossman Family Charitable Foundation
- Gatsby Charitable Foundation
- Kavli Foundation
- Searle Scholars Program
- Human Frontier Science Program
- McKnight Memory and Cognitive Disorders Award
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Episodic memory requires linking events in time, a function dependent on the hippocampus. In trace'' fear conditioning, animals learn to associate a neutral cue with an aversive stimulus despite their separation in time by a delay period on the order of tens of seconds. But how this temporal association forms remains unclear. Here we use two-photon calcium imaging of neural population dynamics throughout the course of learning and show that, in contrast to previous theories, hippocampal CA1 does not generate persistent activity to bridge the delay. Instead, learning is concomitant with broad changes in the active neural population. Although neural responses were stochastic in time, cue identity could be read out from population activity over longer timescales after learning. These results question the ubiquity of seconds-long neural sequences during temporal association learning and suggest that trace fear conditioning relies on mechanisms that differ from persistent activity accounts of working memory.
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