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Mouse Study: Neuron Growth in Adult Brain Buffers Stress

Mouse Study: Neuron Growth in Adult Brain Buffers StressThe effects of stress are lessened through the growth of new neurons in the adult brain, according to a National Institute of Mental Health (NIMH) mouse study. Prior research has shown that neurogenesis — the growth of new neurons — in adults aids in depression recovery.   This suggests that a lack of new neurons is involved in the development of depression.

The hippocampus — where neurogenesis is known to occur — plays a strong role in learning and memory and also helps regulate the stress response.  Research has shown that stress (a risk factor for depression) and the hormones released during a stressful experience reduce the rate of neurogenesis in the hippocampus.

Other research has shown that currently available antidepressants enhance neurogenesis, and so does exercise, also proven to help build resiliency to stress.

Significantly, although there is much evidence pointing to a link between neurogenesis and depression, research has shown that when neurogenisis in animals has been artificially prevented, the animals did not develop depressive behaviors. This suggested that altered neurogenesis wouldn’t directly cause depression; the NIMH study was designed to explore this connection.

In this study, NIMH intramural scientists led by Heather Cameron interrupted adult neurogenesis in mice, then observed how the mice responded to stress.

During the study, it appeared as if the mice had an impaired response to stress when neurogenesis was missing. For example, in the first test, scientists used gene transfer to make newly growing neurons susceptible to an antiviral drug, so that the newly dividing, but immature neurons, were removed. The researchers then compared how mice with and without adult neurogenesis handled the stress of being restrained.

Just after the restraint was over, both groups of mice had similar levels of the hormone corticosterone, a sign of stress. However, thirty minutes later corticosterone was still higher in the mice without adult neurogenesis, suggesting that the ability to recover from stress had been altered.  Also, it was shown that neurogenesis specifically in the hippocampus (and not other areas of the brain) had altered the stress response.

In another standard test of depression-like behavior, food was placed in an open, exposed space, and scientists observed whether the mice would venture out to get some food.

Mice that had not undergone any stress responded similarly regardless of whether neurogenesis was intact. However, mice whose neurogenesis had been impaired and had also undergone the stress of being restrained took longer to eat, choosing safety over food. These and other tests suggested that the presence or absence of neurogenesis affected how the mice reacted to stress, regarding both hormonal responses as well as behavior.

Stress is a strong risk factor for depression, but certain individuals seem particularly susceptible to stress while others seem more resilient. This work suggests that adult neurogenesis helps an individual better handle stress. Therefore, stress itself may trigger a cycle that spirals into a declining ability to effectively handle more stress, possibly leading to depression.

Understanding how adult neurogenesis affects the development of depression—and how it works in the actions of antidepressant drugs—can help with the prevention and treatment of depression.

The findings are published in the journal Nature.

Source:  NIMH

Mouse Study: Neuron Growth in Adult Brain Buffers Stress

Traci Pedersen

Traci Pedersen is a professional writer with over a decade of experience. Her work consists of writing for both print and online publishers in a variety of genres including science chapter books, college and career articles, and elementary school curriculum.

APA Reference
Pedersen, T. (2018). Mouse Study: Neuron Growth in Adult Brain Buffers Stress. Psych Central. Retrieved on November 30, 2020, from
Scientifically Reviewed
Last updated: 8 Aug 2018 (Originally: 21 Aug 2011)
Last reviewed: By a member of our scientific advisory board on 8 Aug 2018
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