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J Neurophysiol (November 1, 2002). 10.1152/jn.00152.2002
Submitted on 4 March 2002
Accepted on 15 July 2002
1Department of Physiological Science, 2Division of Neurosurgery, UCLA Brain Injury Research Center and 3Brain Research Institute, Los Angeles, California 90095
Gómez-Pinilla, Fernando,
Zhe Ying,
Roland R. Roy,
Raffaella Molteni, and
V. Reggie Edgerton.
Voluntary Exercise Induces a BDNF-Mediated Mechanism That
Promotes Neuroplasticity. J. Neurophysiol. 88: 2187-2195, 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), growth-associated 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-A-treated
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.
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