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Published on: July 4, 2013
by April Flowers for Red Orbit:
A new study led by Princeton University reveals physical activity reorganizes the brain so that its response to stress is decreased. This makes anxiety less likely to interfere with normal brain function.
The findings, published in The Journal of Neuroscience, show when regularly exercised mice experienced a stressor – for example, exposure to cold water — their brains exhibited a spike in the activity of neurons that shut off excitement. These neurons are located in the ventral hippocampus, a brain region shown to regulate anxiety.
The researchers believe their findings potentially resolve a discrepancy in research related to the effect of exercise on the brain.
Scientists have not understood the mechanism by which exercise reduces anxiety while also promoting the growth of new neurons in the ventral hippocampus, as these young neurons are typically more excitable. It should mean that exercise results in more anxiety, not less. However, the team found exercise also strengthens the mechanisms that prevent these brain cells from firing.
Elizabeth Gould, Princeton’s Dorman T. Warren Professor of Psychology, notes the impact of physical activity on the ventral hippocampus has not specifically been explored in previous research. The research team was able to pinpoint brain cells and regions vital to anxiety regulation, which may help scientists better understand and treat anxiety disorders.
The findings also reveal that from an evolutionary standpoint, the brain can be extremely adaptive and tailor its own processes to an organism’s lifestyle or surroundings. Gould said a higher likelihood of anxious behavior might have been an adaptive advantage for less physically fit animals. Because anxiety often manifests as avoidant behavior, avoiding potentially harmful situations would increase the possibility of survival for those less capable of responding with a “fight or flight” reaction.
“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,” said Gould, who also is a professor in the Princeton Neuroscience Institute.
One group of mice was given unlimited access to a running wheel for the experiments, while another group had no running wheel. Mice are natural runners who can dash up to 2.5 miles a night when given access to a running wheel. After six weeks of exercise, or exercise deprivation, the mice were exposed to cold water for a brief time.
The research team noticed different behavior in the brains of active and sedentary mice almost immediately. The cold water spurred an increase in “immediate early genes,” or short-lived genes that are rapidly turned on when a neuron fires in the brains of sedentary mice. The active mice lacked these genes, suggesting their brain cells did not immediately leap into an excited state in response to the cold water.
The brains of active mice showed every sign of controlling its reaction to an extent not observed in sedentary mice. A boost of inhibitory neuron activity, known to keep excitable neurons in check, was observed. More of the neurotransmitter gamma-aminobutyric acid, or GABA, which tamps down neural excitement was released at the same time. The researchers also found higher amounts of the protein that packages GABA into little travel pods known as vesicles for release into the synapses of the runner mice.
When the team blocked the GABA receptor that calms neuron activity in the ventral hippocampus, the anxiety-reducing effect of exercise was cancelled out. To achieve this block, the team used the chemical bicuculine, which is used in medical research to block GABA receptors and simulate the cellular activity underlying epilepsy. Bicuculine blocked the mollifying effects of GABA in the active mice when it was applied to the ventral hippocampus.
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