Anxiety is less likely to interfere with the brain activity of mice that exercise regularly, research shows.
When the mice experienced a stressor—exposure to cold water—their brains exhibited a spike in the activity of neurons that shut off excitement in the ventral hippocampus, a brain region shown to regulate anxiety.
These findings potentially resolve a discrepancy in research related to the effect of exercise on the brain—namely that exercise reduces anxiety while also promoting the growth of new neurons in the ventral hippocampus.
Because these young neurons are typically more excitable than their more mature counterparts, exercise should result in more anxiety, not less. Researchers, however, found that exercise also strengthens the mechanisms that prevent these brain cells from firing.
The effect of physical activity on the ventral hippocampus specifically has not been deeply explored, says senior author Elizabeth Gould, a psychology professor at Princeton University.
By doing so, members of Gould’s laboratory pinpointed brain cells and regions important to anxiety regulation that may help scientists better understand and treat human anxiety disorders, she says.
Advantages of anxiety
The research also shows that the brain can be extremely adaptive and tailor its own processes to an organism’s lifestyle or surroundings, Gould notes.
A higher likelihood of anxious behavior may have an adaptive advantage for less physically fit creatures. Anxiety often manifests itself in avoidant behavior and avoiding potentially dangerous situations would increase the likelihood of survival, particularly for those less capable of responding with a “fight or flight” reaction, she adds.
“Understanding how the brain regulates anxious behavior gives us potential clues about helping people with anxiety disorders. It also tells us something about how the brain modifies itself to respond optimally to its own environment,” says Gould.
The researchers found that running prevents the activation of new neurons in response to stress.
For the experiments, one group of mice was given unlimited access to a running wheel and a second group had no running wheel. Natural runners, mice will dash up to 4 kilometers (about 2.5 miles) a night when given access to a running wheel, Gould says. After six weeks, the mice were exposed to cold water for a brief period of time.
The brains of active and sedentary mice behaved differently almost as soon as the stressor occurred, an analysis showed. In the neurons of sedentary mice only, the cold water spurred an increase in “immediate early genes,” or short-lived genes that are rapidly turned on when a neuron fires.
The lack of these genes in the neurons of active mice suggested that their brain cells did not immediately leap into an excited state in response to the stressor.
Instead, the brain in a runner mouse showed every sign of controlling its reaction to an extent not observed in the brain of a sedentary mouse. There was a boost of activity in inhibitory neurons that are known to keep excitable neurons in check.
At the same time, neurons in these mice released more of the neurotransmitter gamma-aminobutyric acid, or GABA, which tamps down neural excitement. The protein that packages GABA into little travel pods known as vesicles for release into the synapse also was present in higher amounts in runners.
The anxiety-reducing effect of exercise was canceled out when the researchers blocked the GABA receptor that calms neuron activity in the ventral hippocampus.
The researchers used the chemical bicuculine, which is used in medical research to block GABA receptors and simulate the cellular activity underlying epilepsy. In this case, when applied to the ventral hippocampus, the chemical blocked the mollifying effects of GABA in active mice.
The National Institute of Mental Health supported the research, which was published in the Journal of Neuroscience.
Source: Princeton University