Botulinum-induced muscle paralysis alters metabolic gene expression and fatigue recovery

Gorin, Fredric A; Herrick, Kevin R.; Froman, Byron E.; Palmer, W. K.; Tait, Robert C.; Carlsen, Richard C.

doi:10.1152/ajpregu.1996.270.1.r238

Cited by 7 publications

(13 citation statements)

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“…The peptide was coupled to keyhole limpet hemocyanin and characterization (described elsewhere) has confirmed that the MGP antibody is isozyme specific (Gorin et al, 1996). Rmo myotubes were briefly fixed in 4% formaldehyde, 0.5% zinc salicylate in normal saline, pH 6.5, for 30 min (Ignacio et al, 1990).…”

Section: Immunohistology With An Mgpmentioning

confidence: 99%

“…Total RNA was extracted from cells grown in 60-mm dishes using guanidinium thiocyanate-phenol-chloroform (Gorin et al, 1996). RNA concentration was determined spectrophotometrically and total RNA (10 g) was electrophoretically size-fractionated through a 1.2% agarose gel containing 2.2 M formaldehyde (Mathews et al, 1998).…”

Section: Rna Isolation and Fractionationmentioning

confidence: 99%

“…The following cDNA probes were hybridized to the RNA blots: (1) the cDNA probe for rat MGP was a 528-bp KpnI/SmaI restriction fragment that corresponds to amino acids 612-821 (Gorin et al, 1996); (2) the mouse ␣ subunit, acetylcholine receptor (␣AChR) cDNA was a 776-bp cDNA fragment generated from AvaI/EcoRI digestion of the 1.76-kb EcoRI restriction fragment present in the pGEM-1 plasmid (American Type Culture Collection, Manassas, VA) (Isenberg, 1986). RNAse protection assays previously demonstrated that this 776-bp fragment annealed selectively to the ␣ subunit transcript in total RNA using hybridization conditions described below (Mathews et al, 1998); (3) the probe for the rat mitochondrially encoded gene, subunit 1 of the nicotinamide dehydrogenase complex (mNAD1), was a 196-bp region amplified from nucleotides 2907-3102 of the mitochondrial genome (Gadaleta et al, 1989); and (4) the mouse ribosomal 18S probe was 100 bp and isolated as an XbaI fragment from the pT7 plasmid (Ambion, Austin, TX) (Mathews et al, 1998).…”

Section: Cdna Probesmentioning

confidence: 99%

“…Neural regulation of MGP transcript in situ appears to be predominantly by nerve-dependent contractile activity rather than by neurotrophic factors. Inhibition of contractile activity with either botulinum A toxin (BTX) or tetrodotoxin (TTX) reduced MGP mRNA levels to 30% of control levels after 7 days (Gorin et al, 1996;Mathews et al, 1998). This reduction is comparable to that observed 7 days after denervation, and the decrease in MGP mRNA levels precedes the reduction in protein levels (Leyland et al, 1990).…”

mentioning

confidence: 99%

“…BTX and TTX are highly selective neurotoxins that inhibit neuromuscular activity by different mechanisms. BTX inhibits presynaptic neurotransmitter release at the neuromuscular junction, whereas TTX was used to block neural transmission of the proximal sciatic nerve without affecting axonal transport (Gorin et al, 1996;Mathews et al, 1998). Selective inhibition of axonal transport with vinblastine did not alter MGP expression in TA muscle except at increased dosages where nerve-evoked contractile activity was impaired (Mathews et al, 1998).…”

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confidence: 99%

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Role of the sarcoplasmic reticulum in regulating the activity-dependent expression of the glycogen phosphorylase gene in contractile skeletal muscle cells

et al. 2000

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Nerve-evoked contractile activity in skeletal muscle regulates transcript and protein levels of many metabolic genes in a coordinate fashion, including the muscle isozyme of glycogen phosphorylase (MGP). Cellular signaling mechanisms mediating the activity-dependent modulation of MGP transcript levels were investigated in a spontaneously contractile rat skeletal muscle cell line (Rmo). Mechanisms regulating MGP mRNA levels in Rmo myotubes were compared with those previously shown to modulate the gene encoding the alpha subunit of the acetylcholine receptor (alphaAChR). Reducing the resting membrane potential from -78 to -30 mV, either electrochemically (KCl) or by increasing Na(+) permeability (veratridine): (1) prevented activation of transverse tubules, (2) impeded calcium release by the sarcoplasmic reticulum (SR), and (3) blocked Rmo contractility. MGP mRNA levels decreased to 30% of control levels and alphaAChR levels increased to 350% following 24 h of depolarization. Differing mechanisms appear to mediate this voltage-dependent regulation of MGP and alphaAChR. Inhibition of SR calcium efflux selectively decreased MGP mRNA levels by 30-50% when using dantrolene, thapsigargin, or a dose of ryanodine shown to inactivate Ca(2+)-induced SR Ca(2+) release (CICR). By contrast, blockade of voltage sensors in transverse tubules with nifedipine, a dihydroaminopyridine (DHAP) antagonist, selectively increased alphaAChR mRNA levels by twofold. These data indicate that the voltage-dependent regulation of AChR gene expression differs from that modulating the MGP gene. KCl-induced depolarization and dantrolene both inhibit pulsatile SR Ca(2+) efflux in Rmo myotubes, but by differing mechanisms. Depolarization and dantrolene comparably reduced MGP mRNA levels and decreased MGP transcript stability from a t(1/2) of 24 h to 14.5 and 16 h, respectively. Reduced transcript stability can account for the observed reduction in mRNA levels of MGP in noncontractile Rmo myotubes and could be a significant regulatory mechanism in skeletal muscle that coordinates the activity-dependent expression of MGP with other glycogenolytic genes.

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Section: Immunohistology With An Mgpmentioning

confidence: 99%

Section: Rna Isolation and Fractionationmentioning

confidence: 99%

Section: Cdna Probesmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Role of the sarcoplasmic reticulum in regulating the activity-dependent expression of the glycogen phosphorylase gene in contractile skeletal muscle cells

et al. 2000

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Dramatic changes in muscle contractile and structural properties after 2 botulinum toxin injections

et al. 2015

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Introduction Botulinum toxin is frequently administered serially to maintain therapeutic muscle paralysis, but repeated dose effects on muscle function are largely unknown. This study characterized the muscle response to 2 onabotulinum toxin (BoNT) injections separated by 3 months. Methods Animal subjects received a single toxin injection (n=8), 2 BoNT injections separated by 3 months (n= 14), or 1 BoNT and 1 saline injection separated by 3 months (n=8). Results The functional effect of 2 serial injections was exponentially greater than the effect of a single injection. While both groups treated with a single BoNT injection had decreased torque in the injected leg by about 50% relative to contralateral legs, the double BoNT injected group had decreased torque by over 95% relative to the pre-injection level. Both single and double BoNT injections produced clear signs of fiber-type grouping. Discussion These experiments demonstrate a disproportionately increased effect of a second BoNT injection.

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A consensus statement on the use of botulinum toxin in pediatric patients

Vova

Green

Brandenburg

et al. 2021

PM&R

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Botulinum toxin has been used in medicine for the past 30 years. However, there continues to be controversy about the appropriate uses and dosing, especially in the pediatric population. A panel of nine pediatric physiatrists from different regions and previous training programs in the United States were nominated based on institutional reputation and botulinum toxin (BoNT) experience. Based on a review of the current literature, the goal was to provide the rationale for recommendations on the administration of BoNT in the pediatric population. The goal was not only to review safety, dosing, and injection techniques but also to develop a consensus on the appropriate uses in the pediatric population. In addition to upper and lower limb spasticity, the consensus also provides recommendations for congenital muscular torticollis, cervical dystonia, sialorrhea, and brachial plexus palsies.

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Botulinum-induced muscle paralysis alters metabolic gene expression and fatigue recovery

Cited by 7 publications

References 0 publications

Role of the sarcoplasmic reticulum in regulating the activity-dependent expression of the glycogen phosphorylase gene in contractile skeletal muscle cells

Role of the sarcoplasmic reticulum in regulating the activity-dependent expression of the glycogen phosphorylase gene in contractile skeletal muscle cells

Dramatic changes in muscle contractile and structural properties after 2 botulinum toxin injections

A consensus statement on the use of botulinum toxin in pediatric patients

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