Motor nerve terminal morphologic plasticity induced by small changes in the locomotor activity of the adult rat

Tomàs, Josep; Fenoll, Rosa; Santafé, Manel M.; Batlle, Jordi de; Mayayo, Emili

doi:10.1016/0304-3940(89)90215-2

Cited by 14 publications

(14 citation statements)

References 12 publications

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“…Here we show evidence of ThR protein at the NMJ in the adult. The presence of ThR in the adult could be related to the activity‐dependent plasticity that occurs normally in adult life (Tomàs et al, 1989, 2000). In accordance with this, denervation of adult muscle resulted in a reversal of the expression levels of the three genes of prothrombin, ThR, and the physiological serine‐protease inhibitor PN‐1, indicating that these genes were regulated in an innervation‐dependent manner and that nerve activity may play an important regulatory role in the expression of prothrombin, ThR, and PN‐1 (Kim et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Role and expression of thrombin receptor PAR‐1 in muscle cells and neuromuscular junctions during the synapse elimination period in the neonatal rat

Lanuza

García

González

et al. 2003

J of Neuroscience Research

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A role for thrombin and its receptor (ThR) during mammalian skeletal muscle cell differentiation and neuromuscular junction (NMJ) formation has been suggested. Previously, we found that the synapse elimination process in the neonatal rat muscle was accelerated by thrombin and blocked by hirudin, its specific inhibitor (Lanuza et al. [2001] J. Neurosci. Res. 63:330-340). To test whether this process resulted from a signal transduction cascade initiated by activation of ThR, in particular PAR-1, we applied to the levator auris longus (LAL) muscle of newborn rats two synthetic peptides (SFLL and FSLL). SFLL is a potent specific agonist for activation of PAR-1, whereas FSLL is an inactive peptide. We have demonstrated that the activation of PAR-1 by SFLL produced acceleration of the presynaptic loss of connections and the postsynaptic maturation of NMJs. Moreover, Western blot analysis showed that PAR-1 was present in the skeletal muscle, and by immunohistochemistry we detected PAR-1 in muscle fibers concentrated in the synaptic area but also in satellite cells. Several lines of evidence suggested that PAR-1 is localized in the postsynaptic membrane: PAR-1 immunofluorescence was concentrated at denervated synaptic sites and was present in the myotube membrane in vitro in the absence of neurons and in dissociated single muscle fibers from which nerve terminals and Schwann cells had been removed. Taken together, these results indicate that thrombin mediates certain stages of activity-dependent synapse elimination in the skeletal muscle and does so through its action on the thrombin receptor PAR-1 localized, at least in part, on the postsynaptic membrane.

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Section: Discussionmentioning

confidence: 99%

Role and expression of thrombin receptor PAR‐1 in muscle cells and neuromuscular junctions during the synapse elimination period in the neonatal rat

Lanuza

García

González

et al. 2003

J of Neuroscience Research

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“…The junction dimensions increased in the mouse diaphragm after exposure to hypobaric hypoxia (Appell 1984), but was variably increased in Correspondence to: O. W~erhaug different rat muscles in response to treadmill running (Mytskan 1977). Endurance exercise increased the nerve terminal dimensions and the number of nerve terminal branches more in the adult rat extensor digitorum longus than in the soleus muscle (Andonian and Fahim 1988), but reduced the nerve terminal length and branch number in the extensor digitorum longus of young rats (Tomas et al 1989). Increased number of preterminal axon branches in the soleus muscle, but unchanged number in the gastrocnemius muscle (Stebbins et al 1985) were reported in the rat as response to treadmill training.…”

Section: Introductionmentioning

confidence: 99%

Different effects of physical training on the morphology of motor nerve terminals in the rat extensor digitorum longus and soleus muscles

1992

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The morphology of nerve terminals in the rat extensor digitorum longus and soleus muscles was studied with light microscopy in 13-week-old male animals after 6 weeks of treadmill running and compared with data from untrained controls. The terminals were stained with methylene blue. Physical training tended to increase the area and length of the nerve terminals in relation to the corresponding muscle fiber diameter, and to reduce the density of nerve terminal varicosities, but significant differences between the trained group and the control group were obtained only in the extensor digitorum longus muscle. The different degrees of effect on the nerve terminals in the two muscles may be due to different abilities to respond to the training, but may also be due to differences in work load caused by the training. The effect of training on extensor digitorum longus junctions may reflect some transformation from fast to slow morphological characteristics.

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“…Increased physical activity increases size and degree of branching of motor nerve terminals at neuromuscular junctions of type I fibers,1, 10 increases expression of acetylcholinesterase,24 increases expression of acetylcholine receptor,9 and increases size and density of pre‐ and post‐synaptic membrane specializations 25, 27. There are differential effects on soleus neuromuscular junction morphology based on intensity of training 10.…”

mentioning

confidence: 99%

GDNF is regulated in an activity‐dependent manner in rat skeletal muscle

2002

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Glial cell line-derived neurotrophic factor (GDNF) is produced by skeletal muscle and affects peripheral motor neurons. Elevated expression of GDNF in skeletal muscle leads to hyperinnervation of neuromuscular junctions, whereas postnatal administration of GDNF causes synaptic remodeling at the neuromuscular junction. Studies have demonstrated that altered physical activity causes changes in the neuromuscular junction. However, the role played by GDNF in this process in not known. The objective of this study was to determine whether changes in neuromuscular activity cause altered GDNF content in rat skeletal muscle. Following 4 weeks of walk-training on a treadmill, or 2 weeks of hindlimb unloading, soleus, gastrocnemius, and pectoralis major were removed and analyzed for GDNF content by enzyme-linked immunosorbant assay. Results indicated that walk-training is associated with increased GDNF content. Skeletal muscle from hindlimb-unloaded animals showed a decrease in GDNF in soleus and gastrocnemius, and an increase in pectoralis major. The altered production of GDNF may be responsible for activity-dependent remodeling of the neuromuscular junction and may aid in recovery from injury and disease.

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Motor nerve terminal morphologic plasticity induced by small changes in the locomotor activity of the adult rat

Cited by 14 publications

References 12 publications

Role and expression of thrombin receptor PAR‐1 in muscle cells and neuromuscular junctions during the synapse elimination period in the neonatal rat

Role and expression of thrombin receptor PAR‐1 in muscle cells and neuromuscular junctions during the synapse elimination period in the neonatal rat

Different effects of physical training on the morphology of motor nerve terminals in the rat extensor digitorum longus and soleus muscles

GDNF is regulated in an activity‐dependent manner in rat skeletal muscle

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