Socially isolated mice also showed evidence of greater inflammation in the hippocampus, when compared to socially housed and control mice.
"There was a runaway inflammatory response in the tissue of socially isolated mice, which is damaging to the brain," said Randy Nelson, a co-author of the study and professor of psychology and neuroscience at Ohio State.
Socially isolated mice showed increased activation of microglia, a type of immune cell in the central nervous system that responds to damaged neurons, the study found.
One of the ways microglia respond is by releasing tumor necrosis factor alpha (TNF-a), one of a large family of proteins called cytokines -- chemical messengers that are mobilized when the body is injured or has an infection. These cytokines cause inflammation in their effort to repair an injured or infected area of the body.
Levels of TNF-a were elevated in isolated mice, but not in socially housed mice, compared to the control mice.
The higher levels of TNF-a in the socially isolated mice, and the inflammation it caused, was the main reason for the increased neuronal damage in these animals, Nelson said.
"Inflammation is normally good, but in this case it is too much of a good thing," he said.
In addition, results showed that the isolated mice had higher levels of the stress hormone corticosterone following the heart attack. Other studies have linked elevated levels of this hormone to increased neuronal damage.
"We found that the hormonal stress response network is more activated after cardiac arrest in socially isolated animals," said Courtney DeVries, in whose lab the work was conducted and another co-author and associate professor of psychology and neuroscience at Ohio State.
"This is contributing to damage in the neurons."
| Contact: Courtney DeVries Devries.14@osu.edu 614-292-7353 Ohio State University Source:Eurekalert |