Neurotrophin 4/5 is required for the normal development of the slow muscle fiber phenotype in the rat soleus

Carrasco, Darío I.; English, Arthur W.

doi:10.1242/jeb.00412

Cited by 22 publications

(14 citation statements)

References 37 publications

(37 reference statements)

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“…Such retrograde mechanisms have been studied in detail with respect to neurotrophins (Zweifel et al, 2005). In fact, the neurotrophin NT4 (NTF5 -Mouse Genome Informatics) is a promising candidate retrograde factor; it is selectively expressed by slow muscles and can induce both the growth of motor axons and the differentiation of muscle fibers (Funakoshi et al, 1995;Carrasco and English, 2003). In our hands, delivery of NT4 to developing muscle failed to affect the frequency of SV2A-positive nerve terminals (J.V.C.…”

Section: Retrograde Signal From Muscle To Nervementioning

confidence: 84%

Retrograde influence of muscle fibers on their innervation revealed by a novel marker for slow motoneurons

et al. 2010

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SUMMARYMammalian limb and trunk skeletal muscles are composed of muscle fibers that differ in contractile and molecular properties. They are commonly divided into four categories according to the myosin heavy chain that they express: I, IIA, IIX and IIB, ranging from slowest to fastest. Individual motor axons innervate tens of muscle fibers, nearly all of which are of the same type. The mechanisms accounting for this striking specificity, termed motor unit homogeneity, remain incompletely understood, in part because there have been no markers for motoneuron types. Here we show in mice that the synaptic vesicle protein SV2A is selectively localized in motor nerve terminals on slow (type I and small type IIA) muscle fibers; its close relatives, SV2B and SV2C, are present in all motor nerve terminals. SV2A is broadly expressed at birth; fast motoneurons downregulate its expression during the first postnatal week. An inducible transgene incorporating regulatory elements from the Sv2a gene permits selective labeling of slow motor units and reveals their composition. Overexpression of the transcriptional co-regulator PGC1a in muscle fibers, which converts them to a slow phenotype, leads to an increased frequency of SV2A-positive motor nerve terminals, indicating a fiber type-specific retrograde influence of muscle fibers on their innervation. This retrograde influence must be integrated with known anterograde influences in order to understand how motor units become homogeneous.

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Section: Retrograde Signal From Muscle To Nervementioning

confidence: 84%

Retrograde influence of muscle fibers on their innervation revealed by a novel marker for slow motoneurons

et al. 2010

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“…This difference could be explained by significant fiber atrophy in P2X 2 Ϫ/Ϫ muscle secondary to reduced activity. Reliable neurotransmission is also important in directing muscle fiber typing (Carrasco and English, 2003). The transition from fast to slow type muscle fibers is induced by increased muscle activation during development (Kugelberg, 1976).…”

Section: Discussionmentioning

confidence: 99%

Abnormalities in neuromuscular junction structure and skeletal muscle function in mice lacking the P2X2 nucleotide receptor

et al. 2007

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Abstract-ATP is co-released in significant quantities with acetylcholine from motor neurons at skeletal neuromuscular junctions (NMJ). However, the role of this neurotransmitter in muscle function remains unclear. The P2X 2 ion channel receptor subunit is expressed during development of the skeletal NMJ, but not in adult muscle fibers, although it is reexpressed during muscle fiber regeneration. Using mice deficient for the P2X 2 receptor subunit for ATP (P2X 2 ؊/؊ ), we demonstrate a role for purinergic signaling in NMJ development. Whereas control NMJs were characterized by precise apposition of pre-synaptic motor nerve terminals and postsynaptic junctional folds rich in acetylcholine receptors (AChRs), NMJs in P2X 2 ؊/؊ mice were disorganized: misapposition of nerve terminals and post-synaptic AChR expression localization was common; the density of post-synaptic junctional folds was reduced; and there was increased end-plate fragmentation. These changes in NMJ structure were associated with muscle fiber atrophy. In addition there was an increase in the proportion of fast type muscle fibers. These findings demonstrate a role for P2X 2 receptor-mediated signaling in NMJ formation and suggest that purinergic signaling may play an as yet largely unrecognized part in synapse formation. © 2007 IBRO. Published by Elsevier Ltd. All rights reserved.Key words: ATP, acetylcholine, knockout, mouse, nerve terminal, synapse.It is well established that ATP is co-released with acetylcholine (ACh) from motor nerve terminals (Redman and Silinsky, 1994;Redman and Silinsky, 1996). While ACh is the transmitter that mediates via nicotinic receptors muscle contraction in mature animals, during early development both ATP, acting via P2X ion channel receptors (Ralevic and Burnstock, 1998) and ACh mediate muscle responses (Kolb and Wakelam, 1983;Henning, 1997;Heilbronn and Eriksson, 1998). P2X 2 receptor subunits are expressed during early postnatal development, when neuromuscular junction (NMJ) maturation and patterning occur, but disappear in the adult (Ryten et al., 2001). Furthermore, this receptor is re-expressed in the later stages of muscle regeneration in the mdx mouse model of muscular dystrophy (Ryten et al., 2004;Jiang et al., 2005). Also direct postjunctional responses to ATP reappear after denervation of chick skeletal muscle (Wells et al., 1995).Electrophysiology, immunohistochemistry and reverse transcriptase polymerase chain reaction have demonstrated the expression of a range of purinoceptors in developing skeletal muscle, including P2X 2 , P2X 5 , P2X 6 , P2Y 1 , P2Y 2 and P2Y 4 (Kolb and Wakelam, 1983;Hume and Thomas, 1988;Thomas et al., 1991;Henning et al., 1992; Meyer et al., 1999a,b;Bo et al., 2000;Ruppelt et al., 2001;Ryten et al., 2001;Cheung et al., 2003). Specific roles in skeletal muscle fiber formation and function have been identified for two of these receptors. While activation of the P2Y 1 receptor has been shown to regulate acetylcholine receptor (AChR) and acetylcholinesterase (AChE) expression at NMJs...

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“…However, in other studies it was reported that CNTF exerts catabolic and cachectic eVects on innervated muscles (see Espat et al 1996;Martin et al 1996 for references and results), and no eVect on denervated muscles Ramirez et al 2003), with a relative increase in the mass of denervated compared to the contralateral innervated muscle, which appears to be entirely due to the weight loss of the second . Many trophic eVects observed in innervated muscles with the administration of CNTF or other neurotrophic agents are most probably the result of an action on motoneurons, rather than of a direct action on muscles (Carrasco and English 2003;Fraysse et al 2000;Mousavi et al 2002Mousavi et al , 2004Ramirez et al 2003;Vergara and Ramirez 2004). Recently Talon et al (2005) demonstrated that the in vitro application of CNTF induces a rapid inhibition of sodium currents in native dissociated skeletal muscle Wbers, which could modify sarcolemma excitability, so indirectly modifying contractile properties.…”

Section: Muscle Trophism Myowbrillar and Contractile Propertiesmentioning

confidence: 99%

The denervated muscle: facts and hypotheses. A historical review

2006

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Denervation changes in skeletal muscle (atrophy; alterations of myofibrillar expression, muscle membrane electrical properties, ACh sensitivity and excitation-contraction coupling process; fibrillation), and their possible causes are reviewed. All changes can be counteracted by muscle electrostimulation, while denervation-like effects can be caused by the complete conduction block in muscle nerve. These results do not support the hypothesis that the lack of neurotrophic, non-motor factors plays a role in denervation phenomena. Instead they support the view that the lack of neuromotor discharge is the only cause of the phenomena and that neuromotor activity is an essential factor in regulating muscle properties. However, some experimental results cannot apparently be explained by the lack of neuromotor impulses, and may still suggest that neurotrophic influences exist. A hypothesis is that neurotrophic factors, too feeble to maintain a role in completely differentiated, adult muscles, can concur with neuromotor activity in the differentiation of immature, developing muscles.

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Neurotrophin 4/5 is required for the normal development of the slow muscle fiber phenotype in the rat soleus

Cited by 22 publications

References 37 publications

Retrograde influence of muscle fibers on their innervation revealed by a novel marker for slow motoneurons

Retrograde influence of muscle fibers on their innervation revealed by a novel marker for slow motoneurons

Abnormalities in neuromuscular junction structure and skeletal muscle function in mice lacking the P2X2 nucleotide receptor

The denervated muscle: facts and hypotheses. A historical review

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