Exercise increases BDNF levels in the striatum and decreases depressive-like behavior in chronically stressed rats

Abstract

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.

Effects of Aerobic Exercise on Anxiety Disorders: A Systematic Review

“…Though, one of the mechanisms observed with CBT, tailored to the needs of each patient, is the power to produce volumetric changes in the amygdala, in the case of chronic anxiety [48]. Human studies have shown that a deficiency in the availability of BDNF is associated with vulnerability to depression [49] and this deficiency is reduced after 30 minutes of exercise in patients with panic disorder but not in healthy controls [50] Another mechanism is influenced by exercise Increased the brain growth factor such as brainderived neurotrophic factor (BDNF) expression is related to the effects of exercise on brain plasticity, cognitive functioning and health [51,52].…”

The Role of Synapsin I in Intracellular Signaling Mechanisms Underlies Exercise-Induced Improvement in Social Memory: A Systematic Review

“…In all the 12 studies, the scholars agreed in unison that synapsin I plays a significant role in initiating the intracellular signaling mechanism. In one study, 1 week long of enforced physical exercise has the capacity of improving the social memory in a characteristically troubling dimensional activity appertaining to the augmentation of the corresponding to the manifestation of the brain derivative neurological factor in the dentate gyrus, hippocampus, and the perirhinal cortex [12]. The other studies revealed that the administration of a single dosage of BDNF in the intracellular cerebral ventricle is adequate to emulate the developments in the object identification.…”

Comparison Among Aerobic Exercise and Other Types of Interventions to Treat Depression: A Systematic Review

“…Human studies have shown that a deficiency in the availability of BDNF is associated with vulnerability to depression [85]. The Increased the brain growth factor such as BDNF expression is related to the effects of exercise on brain plasticity, cognitive functioning and health [27,58].…”