Exercise increases BDNF levels in the striatum and decreases depressive-like behavior in chronically stressed rats.
Early life stress in humans can affect the development of neurons and neurotransmitter systems and predispose an individual to the subsequent development of depression. Similarly, in rats, maternal separation causes anxiety and depressive-like behavior and decreased corticosterone levels. Patients receiving pharmacological treatment for depression often experience negative side-effects or do not respond optimally and therefore the use of exercise as alternative antidepressant treatment is investigated. The aim of the study was to see whether rats subjected to both early life stress and chronic stress later in life show differences in depressive-like behavior, neurotrophin levels, stress hormone levels and antioxidant capacity of serum after chronic voluntary exercise as treatment. Rat pups were maternally separated and one group were allowed access to running wheels for 6 weeks while control rats were also handled and put in cages without running wheels. All rats were subjected to chronic restraint stress during adulthood. A forced swim test was done to test for depressive-like behavior. Neurotrophins were measured in the ventral hippocampus and striatum; baseline stress hormones were measured in blood plasma as well as the anti-oxidative potential of serum. Compared to controls, rats that exercised had no difference in baseline stress hormones, but had decreased immobility times in the forced swim test, increased brain derived neurotrophic factor (BDNF) levels in the striatum and decreased anti-oxidative potential of their serum. The mechanism by which depressive-like behavior was improved may have been mediated through increased striatal BDNF levels, resulting in increased neuroplasticity and the prevention of neuronal death.
Division of Medical Physiology, Stellenbosch University, Tygerberg, PO Box 19063, 7505, South Africa. lrichter@sun.ac.za
Lelanie
L
Marais
Dan J
DJ
Stein
Willie M U
WM
Daniels
D000367:Age Factors; D000375:Aging / Q000502:physiology; D000818:Animals; D000975:Antioxidants / Q000032:analysis / Q000378:metabolism; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D002908:Chronic Disease; D003342:Corpus Striatum / Q000254:growth & development / Q000378:metabolism* / Q000503:physiopathology; D003866:Depressive Disorder / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy*; D004195:Disease Models, Animal; D005081:Exercise Therapy / Q000379:methods*; D006854:Hydrocortisone / Q000032:analysis / Q000097:blood; D008297:Male; D009410:Nerve Degeneration / Q000503:physiopathology / Q000517:prevention & control; D009473:Neuronal Plasticity / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012149:Restraint, Physical / Q000502:physiology / Q000523:psychology; D013315:Stress, Psychological / Q000150:complications / Q000503:physiopathology*; D013550:Swimming / Q000502:physiology / Q000523:psychology; D013995:Time; D015854:Up-Regulation / Q000502:physiology
D000975:Antioxidants; D019208:Brain-Derived Neurotrophic Factor; D006854:Hydrocortisone