Voluntary Exercise Induces a BDNF-Mediated Mechanism That Promotes Neuroplasticity

FERNANDO GO´MEZ-PINILLA,1,2 ZHE YING,1 ROLAND R. ROY,3 RAFFAELLA MOLTENI,1 AND V. REGGIE EDGERTON1,3 1Department of Physiological Science, 2Division of Neurosurgery, UCLA Brain Injury Research Center and 3Brain Research Institute, Los Angeles, California 90095 Received 4 March 2002; accepted in final form 15 July 2002 “BDNF is a powerful modifier of neuronal excitability and synaptic transmission”. The authors were interested to determine whether exercise induces an integrated response of BDNF and its receptors that may lead to synaptic modification at the level of neuromuscular system. To test this, they allowed 3 months old male SD rats to exercise for a period of 3 days and 7 days in running wheel with increasing load over the time period. The authors selected the lumbar region of the spinal cord and soleus muscle to examine the changes since the motor pools innervating the hindlimb muscles are located in the lumbar region of the spinal cord and running involves recruitment of soleus muscle. Further to examine whether muscle activation via locomotion is the main stimulus for the induction of neurotrophins the authors paralyzed the soleus muscle with botulinum toxin in separate groups of animals. Voluntary exercise increased the mRNA expression of synapsin I, which mediates the action of BDNF. Synapsin I mRNA levels were increased in proportion to growth associated protein (GAP-43) and signal transduction receptor (trkB). These suggest that exercise can impact synaptic growth and function. Paralysis of soleus muscle resulted in reduced BDNF and synpasin I mRNA levels suggesting that basal level of neuromuscular activity is necessary to maintain normal levels of BDNF. Overall BDNF was shown to play an important role in exercise mediated neuronal plasticity and function in the neuromuscular system. -Madhan