Dynamics of nerve-muscle interaction in developing and mature neuromuscular junctions

Grinnell, Alan D.

doi:10.1152/physrev.1995.75.4.789

Cited by 123 publications

(71 citation statements)

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“…We hypothesize that the rapid decline in AChR concentration after 5 days postinjury was due to the more rapid recovery of contractile activity compared with the recovery observed following denervation. It is known that there is postsynaptic regulation of AChR density based on studies using chronic NMJ blockade and direct electrical stimulation of denervated muscle (Saltpeter & Loring, 1985;Grinnell, 1995). In those studies, it was not possible to determine whether the attenuated muscle fibre electrical activity per se or the resulting reduction in SR Ca¥ release or mechanical activity was responsible for the increased AChR expression.…”

Section: Discussionmentioning

confidence: 99%

Uncoupling of in vivo torque production from EMG in mouse muscles injured by eccentric contractions

Warren

Ingalls

Shah

et al. 1999

The Journal of Physiology

101

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Section: Discussionmentioning

confidence: 99%

Uncoupling of in vivo torque production from EMG in mouse muscles injured by eccentric contractions

Warren

Ingalls

Shah

et al. 1999

The Journal of Physiology

101

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“…Denervation deprives skeletal muscle of nerve-evoked contractile activity and of motor neuron-derived factors that influence muscle development and maintain trophic interactions between these two tissues (Grinnell, 1995). To investigate factors that might maintain PKC isoform levels in skeletal muscle, we examined PKC isoform expression in rat primary myotube cultures that are not innervated.…”

Section: Discussionmentioning

confidence: 99%

Neural Influence on Protein Kinase C Isoform Expression in Skeletal Muscle

et al. 1996

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Protein kinase C (PKC) is a family of enzymes involved in synapse formation and signal transduction at the neuromuscular junction. Two PKC isoforms, classical PKC ␣ and novel PKC , have been shown to be enriched in skeletal muscle or localized to the endplate. We examined the role of nerve in regulating the expression of these PKC isoforms in rat skeletal muscle by denervating diaphragm muscle and measuring PKC protein expression at various postoperative times. nPKC protein levels decreased 65% after denervation, whereas cPKC ␣ levels increased 80% compared with control hemidiaphragms. These results suggest that innervation regulates PKC and ␣ isoform expression in skeletal muscle. To explore further how nerve regulates PKC expression, we characterized PKC isoform expression in rat myotubes deprived of neural input. Myoblast expression of nPKC was low, and the increase in nPKC expression that occurred during differentiation into myotubes resulted in levels of nPKC significantly below adult skeletal muscle. cPKC ␣ expression in myoblasts increased during differentiation to levels that exceeded expression in adult skeletal muscle. Coculturing myotubes with a neuroblastoma X glioma hybrid clonal cell line (NG108-15) increased nPKC expression, but not cPKC ␣, suggesting that nPKC in skeletal muscle and myotubes is regulated by nerve contact or by a factor(s) provided by nerve. Treating myotubes with tetrodotoxin did not affect either basal-or NG108-15 cell-stimulated nPKC expression. Together these results suggest that expression of nPKC in skeletal muscle is regulated by a transynaptic interaction with nerve that specifically influences nPKC expression.

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“…The origin of AChE in muscle endplates has been an area of long-standing investigation (Anglister and McMahan, 1985;Grinnell, 1995;Rotundo et al, 1997;Jevsek et al, 2004;Mis et al, 2005). Previous work has shown AChE expression in motor neurons to be present along the axon (Massoulie and Bon, 1982;Rotundo and Carbonetto, 1987).…”

Section: Origin Of Acetylcholinesterase In the Neuromuscular Junctionmentioning

confidence: 99%

Acetylcholinesterase Expression in Muscle Is Specifically Controlled by a Promoter-Selective Enhancesome in the First Intron

Camp¹,

Jaco²,

Zhang³

et al. 2008

J. Neurosci.

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Mammalian acetylcholinesterase (AChE) gene expression is exquisitely regulated in target tissues and cells during differentiation. An intron located between the first and second exons governs a ϳ100-fold increase in AChE expression during myoblast to myotube differentiation in C2C12 cells. Regulation is confined to 255 bp of evolutionarily conserved sequence containing functional transcription factor consensus motifs that indirectly interact with the endogenous promoter. To examine control in vivo, this region was deleted by homologous recombination. The knock-out mouse is virtually devoid of AChE activity and its encoding mRNA in skeletal muscle, yet activities in brain and spinal cord innervating skeletal muscle are unaltered. The transcription factors MyoD and myocyte enhancer factor-2 appear to be responsible for muscle regulation. Selective control of AChE expression by this region is also found in hematopoietic lineages. Expression patterns in muscle and CNS neurons establish that virtually all AChE activity at the mammalian neuromuscular junction arises from skeletal muscle rather than from biosynthesis in the motoneuron cell body and axoplasmic transport.

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Dynamics of nerve-muscle interaction in developing and mature neuromuscular junctions

Cited by 123 publications

References 0 publications

Uncoupling of in vivo torque production from EMG in mouse muscles injured by eccentric contractions

Uncoupling of in vivo torque production from EMG in mouse muscles injured by eccentric contractions

Neural Influence on Protein Kinase C Isoform Expression in Skeletal Muscle

Acetylcholinesterase Expression in Muscle Is Specifically Controlled by a Promoter-Selective Enhancesome in the First Intron

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