Self-directed exploration provides a Ncs1-dependent learning bonus

Understanding the mechanisms of memory formation is fundamental to establishing optimal educational practices and restoring cognitive function in brain disease. Here, we show for the first time in a non-primate species, that spatial learning receives a special bonus from self-directed exploration. I...

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Bibliographic Details
Published in:Scientific reports 2015-12, Vol.5 (1), p.17697, Article 17697
Main Authors: Mun, Ho-Suk, Saab, Bechara J, Ng, Enoch, McGirr, Alexander, Lipina, Tatiana V, Gondo, Yoichi, Georgiou, John, Roder, John C
Format: Article
Language:English
Subjects:
Animals
CA3 Region, Hippocampal - metabolism
Calcium
Calcium-binding protein
Cognitive ability
Dentate gyrus
Dentate Gyrus - metabolism
Environment
Exploratory Behavior
Freq protein
Gene Knockdown Techniques
Hippocampus
Learning
Male
Mice, Inbred C57BL
Neuronal Calcium-Sensor Proteins - metabolism
Neuropeptides - metabolism
Nucleus accumbens
Nucleus Accumbens - metabolism
Proto-Oncogene Proteins c-fos - metabolism
Receptors, Dopamine D2 - metabolism
Rodents
Spatial discrimination learning
Spatial Memory
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Summary:Understanding the mechanisms of memory formation is fundamental to establishing optimal educational practices and restoring cognitive function in brain disease. Here, we show for the first time in a non-primate species, that spatial learning receives a special bonus from self-directed exploration. In contrast, when exploration is escape-oriented, or when the full repertoire of exploratory behaviors is reduced, no learning bonus occurs. These findings permitted the first molecular and cellular examinations into the coupling of exploration to learning. We found elevated expression of neuronal calcium sensor 1 (Ncs1) and dopamine type-2 receptors upon self-directed exploration, in concert with increased neuronal activity in the hippocampal dentate gyrus and area CA3, as well as the nucleus accumbens. We probed further into the learning bonus by developing a point mutant mouse (Ncs1(P144S/P144S)) harboring a destabilized NCS-1 protein, and found this line lacked the equivalent self-directed exploration learning bonus. Acute knock-down of Ncs1 in the hippocampus also decoupled exploration from efficient learning. These results are potentially relevant for augmenting learning and memory in health and disease, and provide the basis for further molecular and circuit analyses in this direction.
ISSN:2045-2322
2045-2322
DOI:10.1038/srep17697