Neurobiological and Endocrine Correlates of Individual Differences in Spatial Learning Ability
Author(s) -
Carmen Sandi,
María I. Cordero,
José Joaquín Merino,
Nyika D. Kruyt,
Ciaran M. Regan,
Keith J. Murphy
Publication year - 2004
Publication title -
learning and memory
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.228
H-Index - 136
eISSN - 1549-5485
pISSN - 1072-0502
DOI - 10.1101/lm.73904
Subject(s) - dentate gyrus , neural cell adhesion molecule , psychology , hippocampal formation , neuroscience , water maze , hippocampus , latency (audio) , spatial learning , morris water navigation task , chemistry , adhesion , computer science , cell adhesion , telecommunications , organic chemistry
The polysialylated neural cell adhesion molecule (PSA-NCAM) has been implicated in activity-dependent synaptic remodeling and memory formation. Here, we questioned whether training-induced modulation of PSA-NCAM expression might be related to individual differences in spatial learning abilities. At 12 h posttraining, immunohistochemical analyses revealed a learning-induced up-regulation of PSA-NCAM in the hippocampal dentate gyrus that was related to the spatial learning abilities displayed by rats during training. Specifically, a positive correlation was found between latency to find the platform and subsequent activated PSA levels, indicating that greater induction of polysialylation was observed in rats with the slower acquisition curve. At posttraining times when no learning-associated activation of PSA was observed, no such correlation was found. Further experiments revealed that performance in the massed water maze training is related to a pattern of spatial learning and memory abilities, and to learning-related glucocorticoid responsiveness. Taken together, our findings suggest that the learning-related neural circuits of fast learners are better suited to solving the water maze task than those of slow learners, the latter relying more on structural reorganization to form memory, rather than the relatively economic mechanism of altering synaptic efficacy that is likely used by the former.
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