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How can the stability of a recently acquired memory be improved? Recent findings regarding the importance of theta frequency EEG activity in the hippocampus suggest that entraining neural activity in that frequency band might increase post-encoding waking replay, reinforcing learning-related plasticity. Our previous studies revealed that upregulating postlearning theta power using EEG neurofeedback (NFB) significantly benefitted procedural and episodic memory performance (both immediate and delayed), and may provide optimal conditions for stabilization of new memories. We have now explored whether memory benefits of theta NFB generalize to delayed spatial memory, an additional hippocampus-dependent process. Participants learned to associate object images with locations on a computer screen. NFB was used to enable participants to selectively increase scalp EEG theta power for 30 minutes. Visuo-spatial memory was tested one week later, with the theta NFB participants compared with 2 control groups (beta-augmentation NFB as an active control group, and an additional passive control group that did not engage in NFB). Theta upregulation was found to improve visuo-spatial memory, as reflected in reduced error distances in location marking and faster reaction time for correct answers by the theta group. This supports the contention that theta upregulation immediately after learning strengthens early consolidation of visuo-spatial memory. This intervention could potentially benefit various memory-challenged populations, as well as healthy individuals.

Previous studies indicate that individuals exposed to stress in juvenility are more prone to suffer from stress-related psychopathologies in adulthood. Evidence suggests that exposure to enriched environment (EE) conditions alleviates juvenile stress (JVS) effects. Exposure to stress has been found to affect immune responses to challenges, but whether JVS has long-term effects on inflammatory processes remains unclear. Here, we examined the impact of JVS on inflammatory processes in adulthood, and the effects of exposure to EE conditions. Adult rats exposed to JVS showed elevated levels of blood monocytes after induction of peritoneal inflammation. This was associated with higher concentration of blood chemokine ligand type 2 (CCL2), but lower levels of its receptor, chemokine receptor type 2 (CCR2) on these monocytes, indicating reduced ability of these monocytes to be recruited to the inflammatory site. In accordance, JVS led to reduced levels of recruited macrophages at the peritoneal cavity, as well as a reduced activation ratio for the release of peritoneal interleukin-10 (IL-10) by lipopolysaccharide (LPS) activation. EE conditions, which fully reversed the anxiety-like behavior resulting from exposure to JVS, did not reverse JVS-induced alterations in blood concentration of monocytes or peritoneal macrophages, but affected IL-10 activation ratio. This effect was associated with a compensatory elevation of the peritoneal CCL2-CCR2 axis. Our results demonstrate long-term metaplasticity-like effects of JVS, which alter inflammatory processes in response to immune challenges in adulthood. Our results also raise the possibility that EE does not simply reverse the effects of JVS but rather indirectly modulates its impact.

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