Simons Foundation Funded Research Finds That Neural ‘Tug-Of-War’ May Explain Fragile X Learning Issues
Mice with the genetic defect that causes Fragile X syndrome (FXS) learn and remember normally, but show an inability to learn new information that contradicts what they initially learned, a new study shows. FXS is the most common genetic cause of intellectual disability and autism.
“These findings suggest that neural circuits in FXS may be fundamentally intact but improperly tuned, which results in inflexibility in gaining certain types of knowledge,” says André Fenton, a professor in the Center for Neural Science at New York University and senior author of the paper, which appears in PLOS Biology.
“We now have a better understanding of a cognitive deficit that is characteristic of FXS—excessive recollection of the information that was once accurate and an inability to process corrective material,” Fenton says.
The study focuses on the hippocampus—the part of the brain crucial for memory, especially about space, which requires both encoding and remembering information.
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 the hippocampus—a mapping that pinpointed whether these neurons are encoding current experience into memory or recollecting information from memory...