Herein, we found that there was no correlation between neurogenesis and learning, this discrepancy with other reports [36], [10] could be explained due to the different role of the HIPP in a reward dependent task and a spatial learning.
Previously, the application of transcranial direct current stimulation, oscillating at the frequency of endogenous slow oscillations, during SWS enhanced memory consolidation for a hippocampus dependent task in human subjects and suggested a causal role of SOs for sleep dependent memory consolidation (Marshall et al., 2006).
We show here that compared to WT mice, P2X7R−/− mice exhibit spatial memory deficits in the Y maze, a hippocampal dependent task, whereas their memory performance was intact in an object recognition paradigm.
This can be conducted by evaluating how good are computed communities for realizing a given dependent task.
Nevertheless, there is no information whether a reward dependent task could induce neurogenesis.
Although cell survival by learning has been previously reported in other paradigms [49], this is the first evidence that showed learning-induced survival in a reward dependent task.
Our group showed for the first time that a reward dependent task differentially induces cell proliferation, cell survival, astrogliogenesis, neurogenesis and neuronal maturation in the mPFC-HIPP circuit.
Mice in which Rac3 is genetically deleted are viable, learn a hippocampal dependent task normally, and have normal dendritic spine densities, although this may be due to compensation by Rac1 [75], [75].
Choosing the best implementation method from paper-based, computerized, and computer generated is a situationally dependent task and medical record and workflow considerations for specific settings should be taken into account.
However, one must consider more than just sheer resolution of the unit, as ultrasound imaging is an operator dependent task that involves optic nerve sheath interpretation, caliper measurement, and ease of software and probe usage.
Similarly, 5-HT7R is necessary for hippocampal-dependent functions [ 55], and the activation of this receptor reversed memory deficits on a hippocampal-dependent task in a mouse model of Rett syndrome [ 99].
