Researchers at the Charlie Norwood VA Medical Center and Georgia State University have shown, using rats, that inflammatory pain at birth changes how the hippocampus works later in life. The change leads to eating more frequently, and in larger amounts.

Recent studies by the same group and others suggest that memory is related to eating habits. Researchers have found that when people don't remember a meal as well – for example, because they were distracted by watching television – they eat more at the next meal. It appears that creating memories of a meal is related to signals sent within the body that the person is full and doesn't need to eat more. The new study further explored this link and showed that a single instance of pain may change how the hippocampus forms memories and therefore alter eating habits for a life span.

Dr. Almira Vazdarjanova, one of the study authors and a researcher with the Charlie Norwood VA Medical Center in Augusta, Georgia, says, "It is somewhat shocking that a single inflammatory event at a critical developmental period can have such lasting influences throughout life."

The results appeared in a May 2017 issue of the journal Physiology & Behavior.

Earlier the reserchers found that eating sweet food increased the expression of the activity–regulated cytoskeleton–associated (Arc) protein by hippocampal neurons. Arc protein is a marker of synaptic plasticity, a process necessary for making new memories.

When hippocampal functioning is impaired, both humans and rats tend to eat more. Another 2017 study by the same research team showed that suppressing the activation of hippocampal neurons in rats caused them to eat more of a sucrose solution and also to return for feeding more frequently. When these neurons are less active, the rats eat more.

The new study took a closer look at the relationship between the hippocampus and eating habits. The researchers caused inflammatory pain in the paws of rats on the day of their birth. They then looked at how this affected the frequency of the rats' consumption of a sucrose solution and how much they ate at each feeding.

The results showed that both male and female rats that had experienced neonatal pain ate more of the sucrose solution at each meal than rats not subjected to pain. The female rats subjected to neonatal pain also showed fewer cells expressing Arc when consuming the sucrose, showing that their hippocampi were functioning differently. The decrease in Arc expression means that fewer neurons were involved in encoding the memory, explains Vazdarjanova.

The researchers also treated some of the rats with morphine after subjecting them to inflammatory pain. Rats that had been given morphine did not show the same eating increases as pain–inflicted rats that were not treated. These results together suggest that the changes in eating behavior were due to the actual experience of pain. It appears that a single instance of inflammatory pain early in life promoted the consumption of pleasing food and disrupted the formation of meal–related memories later in life.

Although the study involved only rats, it has implications for how memory and eating are related in humans as well, say the researchers. The newborn rats used are comparable to a third–trimester human infant in terms of brain development. Thus, inflammatory pain on the day of birth for the rats can be used as a model for premature human infants born into a neonatal intensive care unit (NICU). Premature babies in the NICU often undergo multiple painful procedures every day. Many of these procedures are performed without analgesia. The findings of this study could explain why that is. It may be that early–life stress and trauma experienced in the NICU lead to eating more pleasing foods later in life, the researchers explain.