However, because the same neurons are active in both encoding and remembering, it's unknown what neural events control whether hippocampal neurons are encoding current experience into memory or recollecting information from memory. This dynamic is one of the keys to better understanding FXS, which impairs use of memory in multiple ways.

To explore this, first the scientists had to uncover an electrophysiological "signature of recollection" in hippocampus--a mapping that pinpointed whether these neurons are encoding current experience into memory or recollecting information from memory.

This resulted in two primary findings.

Specifically, they found that encoding and recollection are the result of a neural "tug-of-war" between two distinctive types of rhythmic neural synaptic activity within the hippocampus. Notably, encoding occurs when fast rhythmic activity overwhelms slower rhythmic activity; by contrast, recollection occurs when the slower rhythm dominates the medium rhythm.

The second finding, which sheds new light on FXS, shows that FXS mice have an excessive amount of the slow rhythm.

FXS hippocampus neurons are normal, and, as a result, FXS mice can learn and remember in the ways other mice do. However, due to excessive dominance of the slow rhythm in FXS mice, these mice fail to learn new information that specifically contradicts what they initially learned--in other words, the neural tug-of-war is too often won by the slower rhythm, preventing normal adaptive flexibility of cognitive function.

"This cognitive behavioral inflexibility is characteristic of FXS and autism and now is explained by excessive recollection of the formerly correct but currently incorrect information that is stored in the hippocampus," Fenton observes.



Source: Eurekalert