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BDNF AND NT-4/5 EXPRESSION IN MOUSE PLANTARIS AND SPINAL CORD AFTER FUNCTIONAL OVERLOAD AND VOLUNTARY WHEEL RUNNING

Abstract

PURPOSE: Skeletal muscle is highly plastic and its properties can be modified under varying conditions. Functional overload (FO) of the mouse plantaris by removal of its major synergists results in marked hypertrophy and changes in the biochemical, contractile, and metabolic properties towards those of a “slow” muscle. How these changes are regulated remains largely unknown. Recent studies have shown that some neurotrophic factors, such as brain-derived neurotrophic factor (BDNF) and neurotrophin-4/5 (NT-4/5), regulate the differentiation, survival and maintenance of neurons. In skeletal muscle, these neurotrophic factors are thought to be involved in the adaptation of the neuromuscular system to increased activity. Therefore, we investigated the effects of 1-wk FO with voluntary wheel running exercise (FO-EX) and without voluntary exercise on the expression of BDNF and NT-4/5 in the mouse plantaris muscle and its associated motoneurons. METHODS: Adult female C57BL/6J mice (~4 mos) were assigned to one of three groups: 1) CON; 2) FO, and; 3) FO-EX. Mice in the FO-EX group had free access to a running wheel. Immunohistochemical analyses were performed to assess BDNF protein expression in the plantaris-associated motoneurons, and RT-PCR experiments were performed to quantify BDNF and NT-4/5 mRNA levels in the plantaris muscle. RESULTS: BDNF protein expression in the plantaris-associated motoneurons was 9% and 12% greater (p<0.05) in FO and FO-EX, respectively, compared with age-matched CON. BDNF mRNA expression was higher (p<0.05) in the FO and FO-EX compared to the CON group. The increased expression of BDNF protein and mRNA in the FO-EX group could be due to the distance ran (~23.7 km) during the 1-wk period. In contrast, NT-4/5 mRNA levels in FO and FO-EX were similar to CON. CONCLUSIONS: FO and FO with activity preferentially increased BDNF expression in the plantaris muscle and its motoneurons. NT-4/5 did not respond to FO or FO with activity, implying that BDNF, not NT-4/5, regulates neuronal plasticity during skeletal muscle hypertrophy.

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