Cognitive Flexibility in Mice

Newly-Discovered Gene Mutation Improves Cognitive Flexibility in Mice

A team of U.S. researchers has discovered a genetic mutation that improves cognitive flexibility in mice.

Hu et al reveal a novel mechanism regulating reversal learning and provide potential targets for the treatment of neuropsychiatric disorders characterized by cognitive inflexibility. Image credit: Alexas Fotos.

Electrical signals stimulate chemical messengers that jump from neuron to neuron.

A gene called KCND2 codes for a protein that regulates potassium channels, which control electrical signals that travel along neurons.

Dr. Dax Hoffman from NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development and colleagues found that altering a single base pair in the KCND2 gene enhanced the ability of the protein to dampen nerve impulses.

Mice with this mutation performed better than mice without the mutation in a cognitive task.

The task involved finding and swimming to a slightly submerged platform that had been moved to a new location.

Mice with the mutation found the relocated platform much faster than their counterparts without the mutation.

The scientists now plan to investigate whether the mutation will affect neural networks in the animals’ brains.

“Studying the gene and its protein may ultimately lead to insights on the nature of cognitive flexibility in people,” they said.

“It also may help improve understanding of epilepsy, schizophrenia, Fragile X syndrome, and autism spectrum disorder, which all have been associated with other mutations in KCND2.”

The findings are published in the journal Nature Communications.

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J. Hu et al. 2020. Activity-dependent isomerization of Kv4.2 by Pin1 regulates cognitive flexibility. Nat Commun 11, 1567; doi: 10.1038/s41467-020-15390-x