Learning experiences are potent modulators of adult hippocampal
neurogenesis (AHN). However, the vast majority of findings on the
learning-induced regulation of AHN derive from aversively-motivated
tasks, mainly the water maze paradigm, in which stress is a confounding
factor that affects the AHN outcome. Currently, little is known regarding
the effect of appetitively-motivated training on AHN. Hence we studied
how spatial learning to find food rewards in a hole-board maze modulates
AHN (cell proliferation and immature neurons) and AHN-related hippocampal
neuroplasticity markers (BDNF, IGF-II and CREB phosphorylation) in mice.
The 'Trained' mice were tested for both spatial reference and working
memory and compared to 'Pseudotrained' mice (exposed to different baited
holes in each session, thus avoiding the reference memory component of
the task) and 'Control' mice (exposed to the maze without rewards). In
contrast to Pseudotrained and Control mice, Trained mice reduced the
number of proliferating hippocampal cells but they notably increased
their population of immature neurons assessed by immunohistochemistry.
This evidence shows that hole-board spatial reference learning diminishes
cell proliferation in favor of enhancing young neurons' survival.
Interestingly, the enhanced AHN in the Trained mice (specifically in the
suprapyramidal blade) positively correlated with their reference memory
performance, but not with their working memory. Furthermore, the Trained
animals increased the hippocampal protein expression of all the
neuroplasticity markers analyzed by western blot. Results show that the
appetitively-motivated hole-board task is an useful paradigm to
potentiate and/or investigate AHN and hippocampal plasticity minimizing
aversive variables such as fear or stress.
