To measure anxiety in a mouse and suggest it's similar to anxiety in a person may seem like a stretch, but the metrics sound uncannily familiar.
Paralyzed by fear, afraid to leave the house or socialize with others, scared of new places, preferring the dark to the light of day.
Researchers at The Rockefeller University report this week that mice missing a particular gene show a big increase in these symptomatic behaviors. The scientists also show how the gene, Lynx2, alters the way brain cells communicate and say a similar process may underlie anxiety disorders in humans.
"I'd be surprised if these findings are not relevant to humans," says Nathaniel Heintz, head of the Laboratory of Molecular Biology at Rockefeller, who led the research. "With structures relating to basic functions as evolutionarily ancient as fear and anxiety, I think you can learn a great deal from cross-species studies."
Lynx2 produces molecules that influence communication between neurons in brain areas associated with anxiety. In prior work, the researchers showed that the gene generates a molecule called a mammalian prototoxin, an evolutionary precursor to snake venom toxins. The prototoxins target the same cells as snake venom but regulate their activity instead of inactivating them completely. To investigate exactly what Lynx2 does, Heintz and colleagues knocked out the gene in a line of mice and compared their behavior - and biochemistry - to that of a normal cohort. The bottom line: Mice lacking Lynx2 had no glaring defects, apart from being a very nervous breed.
Compared to regular mice, the jittery creatures spent less time in brightly illuminated spaces, preferring to hide in the dark. They were slower to explore a mysterious new space when presented the option. They chose to isolate themselves in an empty cage rather than socialize with a companion next door.