Literature DB >> 27573800

Effects of Tongue Force Training on Bulbar Motor Function in the Female SOD1-G93A Rat Model of Amyotrophic Lateral Sclerosis.

Delin Ma1, Jeffrey M Shuler2, Aishwarya Kumar2, Quincy R Stanford2, Sudheer Tungtur2, Hiroshi Nishimune2, John A Stanford2.   

Abstract

BACKGROUND: The use of exercise in amyotrophic lateral sclerosis (ALS) is controversial. Although moderate exercise appears to be beneficial for limb muscles in ALS, the effects of exercise on bulbar muscles such as the tongue have not been studied.
OBJECTIVE: To determine the effects of tongue force training on bulbar motor function in the SOD1-G93A rat model of ALS.
METHODS: We compared the effects of tongue force training on bulbar motor function and neuromuscular junction innervation in female SOD1-G93A rats and age-matched female wild-type controls. Half of each group underwent afternoon tongue force training sessions, and all rats were tested under minimal force conditions in the mornings.
RESULTS: Tongue force did not differ between the SOD1-G93A rats and healthy controls during the morning testing sessions, nor was it affected by training. Surprisingly, decreases in tongue motility, the number of licks per session, and body weight were greater in the tongue force-trained SOD1-G93A rats. Forelimb grip force, survival, and denervation of the genioglossus (GG) muscle did not differ between the trained and untrained SOD1-G93A rats. GG innervation was correlated with changes in tongue force but not tongue motility in SOD1-G93A rats at end stage.
CONCLUSIONS: The results indicate a potential deleterious effect of tongue force training on tongue motility in female SOD1-G93A rats. The lack of a relationship between GG innervation and tongue motility suggests that factors other than lower-motor neuron integrity likely accounted for this effect.

Entities:  

Keywords:  animal model; exercise; motor neuron disease; neuromuscular junction

Mesh:

Year:  2016        PMID: 27573800      PMCID: PMC5243852          DOI: 10.1177/1545968316666956

Source DB:  PubMed          Journal:  Neurorehabil Neural Repair        ISSN: 1545-9683            Impact factor:   3.919


  33 in total

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2.  Selective loss of glial glutamate transporter GLT-1 in amyotrophic lateral sclerosis.

Authors:  J D Rothstein; M Van Kammen; A I Levey; L J Martin; R W Kuncl
Journal:  Ann Neurol       Date:  1995-07       Impact factor: 10.422

3.  Knockout of glutamate transporters reveals a major role for astroglial transport in excitotoxicity and clearance of glutamate.

Authors:  J D Rothstein; M Dykes-Hoberg; C A Pardo; L A Bristol; L Jin; R W Kuncl; Y Kanai; M A Hediger; Y Wang; J P Schielke; D F Welty
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4.  Delayed disease onset and extended survival in the SOD1G93A rat model of amyotrophic lateral sclerosis after suppression of mutant SOD1 in the motor cortex.

Authors:  Gretchen M Thomsen; Genevieve Gowing; Jessica Latter; Maximus Chen; Jean-Philippe Vit; Kevin Staggenborg; Pablo Avalos; Mor Alkaslasi; Laura Ferraiuolo; Shibi Likhite; Brian K Kaspar; Clive N Svendsen
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5.  Moderate exercise delays the motor performance decline in a transgenic model of ALS.

Authors:  Isabel Carreras; Sinan Yuruker; Nurgul Aytan; Lokman Hossain; Ji-Kyung Choi; Bruce G Jenkins; Neil W Kowall; Alpaslan Dedeoglu
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6.  Relationships between tongue motility, grip force, and survival in SOD1-G93A rats.

Authors:  Susan E Smittkamp; Heather N Spalding; Jordan W Brown; Hung-Wen Yeh; John A Stanford
Journal:  Physiol Behav       Date:  2013-11-27

7.  Differential regulation of the glutamate transporter variants GLT-1a and GLT-1b in the cortex and spinal cord of transgenic rats expressing hSOD1(G93A).

Authors:  Amélie O Dumont; Emmanuel Hermans; Stéphanie Goursaud
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10.  SOD1 mutants linked to amyotrophic lateral sclerosis selectively inactivate a glial glutamate transporter.

Authors:  D Trotti; A Rolfs; N C Danbolt; R H Brown; M A Hediger
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3.  A Strength Endurance Exercise Paradigm Mitigates Deficits in Hypoglossal-Tongue Axis Function, Strength, and Structure in a Rodent Model of Hypoglossal Motor Neuron Degeneration.

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