Journal
CELL REPORTS
Volume 40, Issue 13, Pages -Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2022.111402
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Funding
- Fonds de Recherche du Quebec Postdoctoral Fellowship [315201]
- National Science Foundation Graduate Research Fellowship
- National Institute of Diabetes and Digestive and Kidney Diseases [DK104897, DK118402, DK118944, DK116558, DK118000]
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Memory of the location of a food or water source is encoded in ventral hippocampus neuron activity and mediated through communication to the lateral septum. This spatial memory is specific to appetitive locations and can be regulated by a specific neural pathway.
Remembering the location of a food or water source is essential for survival. Here, we reveal that spatial mem-ory for food location is reflected in ventral hippocampus (HPCv) neuron activity and is impaired by HPCv lesion. HPCv mediation of foraging-related memory involves communication to the lateral septum (LS), as either reversible or chronic disconnection of HPCv-to-LS signaling impairs spatial memory retention for food or water location. This neural pathway selectively encodes appetitive spatial memory, as HPCv-LS disconnection does not affect spatial memory for escape location in a negative reinforcement procedure, food intake, or social and olfactory-based appetitive learning. Neural pathway tracing and functional map-ping analyses reveal that LS neurons recruited during the appetitive spatial memory procedure are primarily GABAergic neurons that project to the lateral hypothalamus. Collective results emphasize that the neural substrates controlling spatial memory are outcome specific based on reinforcer modality.
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