Differences in the localization of the postsynaptic nitric oxide synthase I and acetylcholinesterase suggest a heterogeneity of neuromuscular junctions in rat and mouse skeletal muscles

Grozdanovic, Zarko; Christova, Tatjana; Gossrau, Reinhart

doi:10.1016/s0065-1281(97)80007-4

Cited by 20 publications

(20 citation statements)

References 26 publications

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“…However, after discovery of the nitric oxide (NO) in the skeletal muscle, the influence of NO and inhibitors of NOS on muscle contractillity was also investigated (2 -4). It is known that the neuronal isoform of NOS (nNOS) is predominantly localized postsynaptically at the neuromuscular junction in the skeletal muscle (5) and that the enzyme responsible for NO production is activated during repetitive contraction of the skeletal muscle. Therefore, during passive incubation, a mouse diaphragm produces approx.…”

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confidence: 99%

NG-Nitro-L-arginine Methyl Ester-Induced Potentiaton of the Effect of Aminophylline on Rat Diaphragm: the Role of Extracellular Calcium

et al. 2004

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Abstract. The role of extracellular calcium in the interaction between intracellular cAMP and nitric oxide (NO)/ cGMP on the contractility of rat diaphragm pretreated with cumulative concentrations of aminophylline (0.36 -3.60 mM) was investigated. In a Ca 2+-free medium, N G -nitro-L-arginine methyl ester (L-NAME) (1 and 3 mM) depressed tension developed (Td) and also aminophylline-induced potentiation of Td in a concentration-dependent manner. Verapamil (2.5 mM) or nicardipine (20 mM) significantly antagonized the potentiating effect of L-NAME on Td in a calcium-containing medium. However, in the presence of verapamil or nicardipine, L-NAME still produced statistically significant potentiation of the cumulative concentrations of aminophylline (0.36 -3.60 mM), given in the second series.

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confidence: 99%

NG-Nitro-L-arginine Methyl Ester-Induced Potentiaton of the Effect of Aminophylline on Rat Diaphragm: the Role of Extracellular Calcium

et al. 2004

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“…More recently, nNOS was shown to be concentrated in the postsynaptic (Grozdanovic et al 1997) and presynaptic regions of normal neuromuscular junctions, where it appears to be located in nerve terminals or Schwann cells of denervated muscle fibres (Ribera et al 1998), or in the Schwann cells of regular inner- Fig. 2.…”

Section: mentioning

confidence: 99%

“…Most of the studies done to establish the localisation of nNOS have used regular immunocytochemistry at the light microscopy level in transverse sections of normal skeletal muscle. However, with this technique insufficient resolution of the pre-and postsynaptic compartments of the nmj is obtained (Grozdanovic et al 1997). In addition, the few immunocytochemical studies at the electron microscopy level have yielded conflicting results about the localisation of nNOS at the neuromuscular junction of normal fibres (Ribera et al 1998 ;Descarries et al 1998).…”

Section: mentioning

confidence: 99%

Immunolocalisation of neuronal nitric oxide synthase at the neuromuscular junction of MDX mice: a confocal microscopy study

2001

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The distribution of nitric oxide synthase at the neuromuscular junction (NMJ) of normal, denervated and mdx mice was studied using a specific antibody against the neuronal isoform of nitric oxide synthase (nNOS). Fluorescence confocal microscopy demonstrated that nNOS immunoreactivity was localised mainly in the sarcolemma and presynaptic region covering acetylcholine receptor branches. The expression of presynaptic nNOS was greatly reduced in dystrophin-deficient muscles. In normal denervated muscles, nNOS was still present in the presynaptic region and there were no qualitative changes in the expression of this protein. These results suggest that the presynaptic distribution of nNOS is associated with terminal Schwann cells. The relationship between nNOS and the presynaptic components of the neuromuscular junction may open new perspectives for improving our understanding of the pathogenesis of dystrophic muscles.

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“…Sarcolemmal neuronal NOS has been shown to be bound to the dystrophin-glycoprotein complex through a N-terminal PDZ protein motif interacting with ␣1-syntrophin, which again binds to the C-terminus of the dystrophin molecule (Adams et al, 1993;Ahn and Kunkel, 1995;Brenman et al, 1996;Watkins et al, 2000). This syntrophin-neuronal NOS complex is highly expressed on the postsynaptic membrane at the neuromuscular junction in most species (Chao et al, 1997;Grozdanovic et al, 1997a;Kusner and Kaminski, 1996;Oliver et al, 1996;Ribera et al, 1998).…”

Section: Constitutive Expression Of Nos Isoforms In Different Speciesmentioning

confidence: 99%

“…Recent studies of NOS and NO in skeletal muscle indicate that altered expression of NOS and production of NO may have manifold consequences for normal muscle development and function as well as for the pathophysiology of muscle fiber damage in neuromuscular diseases Christova et al, 1997;Grozdanovic et al, 1997c;Lee et al, 1994;Silvagno et al, 1996). Especially in muscle fiber innervation, NO and NOS concentrated at the neuromuscular endplate (Chao et al, 1997;Grozdanovic et al, 1997a;, 1996;Oliver et al, 1996) may play a role under normal as well as pathological conditions, which shall be summarized by this short review.…”

Section: Introductionmentioning

confidence: 99%

Role of nitric oxide and nitric oxide synthases in experimental models of denervation and reinnervation

Tews¹

2001

Microscopy Res & Technique

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Nitric oxide (NO) is a short-living free molecule synthesized by three different isoforms of nitric oxide synthases (NOS)-neuronal NOS, endothelial NOS, and inducible NOS-associated with neuromuscular transmission, muscle contractility, mitochondrial respiration, and carbohydrate metabolism in skeletal muscle. Neuronal NOS is constitutively expressed at the muscle fiber sarcolemma linked to the dystrophin-glycoprotein complex and concentrated at the neuromuscular endplate. There is increasing evidence that altered expression of neuronal NOS plays a role in muscle fiber damage in neuromuscular diseases such as dystrophinopathies and denervating disorders. Although there have been some previous conflicting results on the neuronal NOS expression pattern in denervated muscle fibers, it is now well established that denervation is associated with a down-regulation and disappearance of sarcolemmal neuronal NOS at synaptic/extrasynaptic or both sites. As NO has been shown to induce collapse and growth arrest on neuronal growth cones, down-regulation of sarcolemmal neuronal NOS may contribute to axonal regeneration and attraction to muscle fibers aiming at the formation of new motor endplates providing reinnervation and reconstitution of NOS expression. As NO serves as a retrograde messenger, it may trigger structural downstream events responsible for neuromuscular synaptogenesis and preventing polyneural innervation. Nevertheless, decreased NO production in denervation reduces the cytoprotective scavenger function of NO for superoxide anions promoting oxidative stress that is likely to be involved in muscle fiber damage and death. However, the multifaced role of NOS and NO under physiological and pathological conditions remains poorly understood on the basis of the current knowledge.

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Differences in the localization of the postsynaptic nitric oxide synthase I and acetylcholinesterase suggest a heterogeneity of neuromuscular junctions in rat and mouse skeletal muscles

Cited by 20 publications

References 26 publications

NG-Nitro-L-arginine Methyl Ester-Induced Potentiaton of the Effect of Aminophylline on Rat Diaphragm: the Role of Extracellular Calcium

NG-Nitro-L-arginine Methyl Ester-Induced Potentiaton of the Effect of Aminophylline on Rat Diaphragm: the Role of Extracellular Calcium

Immunolocalisation of neuronal nitric oxide synthase at the neuromuscular junction of MDX mice: a confocal microscopy study

Role of nitric oxide and nitric oxide synthases in experimental models of denervation and reinnervation

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