Research ReportEffects of hindlimb unloading on neurotrophins in the rat spinal cord and soleus muscle

- Hindlimb unloading (HU) is used as an experimental disuse model.
- Neurotrophins and their receptors in neuromuscular system are upregulated by HU.
- Results suggest that neurotrophins are involved in HU-induced neuromuscular plasticity.

The aim of the present study was to investigate the effects of hindlimb unloading (HU) on the expression of neurotrophin-3 (NT-3) and brain-derived neurotrophic factor (BDNF), together with the expression of their high-affinity receptors tropomyosin receptor kinase C (TrkC) and tropomyosin receptor kinase B (TrkB), in lumbar (L4-6) segment of the spinal cord and in the soleus muscle. The mRNA and protein levels of the genes of interest were compared using quantitative PCR and western blot assays. Immunohistochemistry for NT-3 and BDNF was used to detect the levels of protein in the motoneurons in the lateral motor column. In this study, NT-3 and BDNF mRNA and protein expression were significantly increased in the spinal cord and soleus muscle after HU. NT-3 immunoreactivity, but not BDNF immunoreactivity, was significantly increased in the large motoneurons located in lateral motor column after 14 days of HU. The level of TrkC protein in the spinal cord and soleus muscle were significantly elevated after both 7 days and 14 days of HU. However, TrkC mRNA, TrkB mRNA and TrkB protein levels did not change significantly. Elevated BDNF, NT-3 and TrkC levels in the neuromuscular system indicate that neurotrophins are involved in HU-induced neuromuscular plasticity. NT-3 is a candidate to mediate the synaptic efficacy between alpha motoneurons and group Ia afferents.