There may be a connection between food comas—resting after eating—and the formation of long-term memories, a team of neuroscientists concludes based on its study on brain activity in sea slugs.
The research appears the Nature Research journal Scientific Reports.
“The sensation of a ‘food coma’ after a hearty meal is well known to anyone who has ever experienced a Thanksgiving dinner,” says Thomas Carew, a professor in New York University’s Center for Neural Science and the paper’s senior author. “In fact, most animals tend to slow down and rest after a large intake of calories, suggesting that there is a biological function to this reaction.
“Our new study proposes that such ‘rest-and-digest’ responses to feeding may have been shaped by evolution to promote the formation of long-term memories.”
The team, which included Nikolay Kukushkin, a postdoctoral fellow in the Carew lab, and Sidney Williams, an NYU undergraduate in Global Liberal Studies at the time of the research, studied Aplysia californica, the California sea slug. Aplysia is a model organism that is powerful for this type of research because its neurons are 10 to 50 times larger than those of higher organisms, such as vertebrates, and it possesses a relatively small network of neurons—characteristics that readily allow for the examination of linkages between neurological and other activity.
In their analysis, the scientists also considered existing scholarship on food intake and the brain.
“In humans, food intake promotes the release of the hormone insulin, which prompts the cells of the body to absorb nutrients from the bloodstream and turn them into fat for long-term storage,” explains Kukushkin. “However, insulin is thought to have little effect on the brain. By contrast, a related hormone, insulin-like growth factor II, has been shown to be critical for proper brain function, including long-term memory formation. However, its release does not depend on calorie intake.
“Therefore, insulin-like molecules in humans are segregated into at least two distinct functional modules. A metabolic module, represented by insulin, controls feeding and energy balance, while a neurotropic module, centered on insulin-like growth factor II, controls memory formation.”
In studying Aplysia, the scientists found that in this species the two distinct modules of insulin-like molecules are, in contrast to humans, unified into a single system that performs both metabolic and neurotropic functions. Moreover, they discovered that a single insulin-like molecule produced in the Aplysia nervous system simultaneously strengthens the contacts between neurons, a mechanism thought to underlie long-term memory, and promotes the absorption of nutrients into the mollusk’s tissues.
The research also involved monitoring the slugs’ behavioral response to food intake—in this case, their regular diet of seaweed.
Here, when animals were allowed to eat their fill, their movement activity was reduced, and this effect was blocked by preventing insulin-like receptors from working.
“Thus, Aplysia’s ‘food coma’ is controlled by their insulin-like system, which acts by redistributing the animal’s energy away from active behavior and towards storage of both nutrients and memory,” observes Carew. “These results will help understand the mechanisms by which insulin and similar molecules elicit both their diet-related and memory-enhancing properties in humans and other animals.”
The researchers note that Aplysia and humans share the general features of the hormone that forms their insulin systems, which evolved in both species to control nutrition, memory, and behavior. However, in Aplysia, these functions have remained unified, while in the human lineage they became partially independent.
“It remains to be established whether the human ‘food coma’ is a vestige of our evolutionary past, or still an important part of memory formation,” Kukushkin acknowledges.
“However, it’s been widely established that in an array of animals, including humans, sleep is well known to be required for proper storage of long-term memories acquired during wakefulness.”
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