Voluntary Exercise Induces a BDNF-Mediated Mechanism That Promotes Neuroplasticity

Abstract

. Voluntary exercise induces a BDNF-mediated mechanism that promotes neuroplasticity. J Neurophysiol 88: 2187Neurophysiol 88: -2195Neurophysiol 88: , 2002 10.1152/jn.00152.2002. We have investigated potential mechanisms by which exercise can promote changes in neuronal plasticity via modulation of neurotrophins. Rodents were exposed to voluntary wheel running for 3 or 7 days, and their lumbar spinal cord and soleus muscle were assessed for changes in brain-derived neurotrophic factor (BDNF), its signal transduction receptor (trkB), and downstream effectors for the action of BDNF on synaptic plasticity. Exercise increased the expression of BDNF and its receptor, synapsin I (mRNA and phosphorylated protein), growthassociated protein (GAP-43) mRNA, and cyclic AMP response element-binding (CREB) mRNA in the lumbar spinal cord. Synapsin I, a synaptic mediator for the action of BDNF on neurotransmitter release, increased in proportion to GAP-43 and trkB mRNA levels. CREB mRNA levels increased in proportion to BDNF mRNA levels. In separate experiments, the soleus muscle was paralyzed unilaterally via intramuscular botulinum toxin type A (BTX-A) injection to determine the effects of reducing the neuromechanical output of a single muscle on the neurotrophin response to motor activity. In sedentary BTX-A-treated rats, BDNF and synapsin I mRNAs were reduced below control levels in the spinal cord and soleus muscle. Exercise did not change the BDNF mRNA levels in the spinal cord of BTX-Atreated rats but further reduced the BDNF mRNA levels in the paralyzed soleus relative to the levels in sedentary BTX-A-treated rats. Exercise also restored synapsin I to near control levels in the spinal cord. These results indicate that basal levels of neuromuscular activity are required to maintain normal levels of BDNF in the neuromuscular system and the potential for neuroplasticity.

Exercise decreases myelin‐associated glycoprotein expression in the spinal cord and positively modulates neuronal growth

“…It is possible that exercise elicits a general increase in BDNF content that may act directly on oligodendrocytes to regulate their functions such as myelin production and maintenance. We have previously reported that exercise increases the expression of BDNF in motorneurons, and glial-like cells in the white matter surrounding motoneuron axons (Gomez-Pinilla et al, 2002). In addition, it has been shown that long-term locomotor training upregulates BDNF and TrkB receptor expression in oligodendrocytes in the spinal cord (Skup et al, 2002).…”

“…For example, physical activity promotes adult neurogenesis (van Praag et al, 1999) and neural healing after CNS injury (Molteni et al, 2004). We have shown that physical activity elevates levels of BDNF in spinal cord areas activated by motor and sensory inputs derived from locomotion (Gomez-Pinilla et al, 2002). In the present studies, we investigated the influence of voluntary exercise on molecular systems responsible for growth inhibition such as MAG.…”

Exercise reverses the harmful effects of consumption of a high-fat diet on synaptic and behavioral plasticity associated to the action of brain-derived neurotrophic factor

“…As the brain can neither synthesize nor store energy reserves, daily diet provides the immediate source of energy to the brain, thereby a means to influence brain function. A diet rich in saturated fat and refined sugar (HF), similar in composition to the average popular diet of most industrialized Western societies, can threaten neuronal plasticity and compromise the capacity of the rodent brain for learning (Greenwood and Winocur, 1996;Winocur and Greenwood, 1999;Molteni et al, 2002). On the other hand, epidemiological studies indicate that exercise can decrease cognitive decay associated to aging (Kramer et al, 1999) and is inherently beneficial for reducing the risk of various diseases (Friedland et al, 2001;Laurin et al, 2001).…”

Age and activity-related changes in the respiratory motor system

“…Neurotrophic factors such as BDNF and GDNF trigger the release of pre-synaptic NRG from nerve terminals 28,29) . Importantly, it is also reported that BDNF and GDNF are stored in vesicles and released with activity, and that NRG controls acetylcholine receptor synthesis at neuromuscular junctions 30,31) .…”