Motor terminal degeneration unaffected by activity changes in SOD1G93A mice; a possible role for glycolysis

Neurobiology of Disease

Volumn 48, Issue 1, 2012, Pages 132-140

  Carrasco, Dario I ^a   Bichler, Edyta K ^b   Rich, Mark M ^c   Wang, Xueyong ^c   Seburn, Kevin L ^d   Pinter, Martin J ^a  

^a EMORY UNIVERSITY   (United States)

^b MOREHOUSE SCHOOL OF MEDICINE   (United States)

^c WRIGHT STATE UNIVERSITY   (United States)

^d JACKSON LABORATORY   (United States)

Author keywords

G93A; Glycolysis; HCSMA; Mitochondria; Motor neuron disease; Motor terminal; Neurodegeneration; SOD1

Indexed keywords

ADENOSINE TRIPHOSPHATE; COPPER ZINC SUPEROXIDE DISMUTASE; GLUCOSE; TETRODOTOXIN;

ANIMAL TISSUE; ARTICLE; COMPARATIVE STUDY; CONTROLLED STUDY; CULTURE MEDIUM; DISEASE COURSE; GENE MUTATION; GENE OVEREXPRESSION; GLYCOLYSIS; HEREDITARY SPINAL MUSCULAR ATROPHY; MINIATURE ENDPLATE POTENTIAL; MITOCHONDRION; MOUSE; MUSCLE CONTRACTION; MUSCLE DENERVATION; MUSCLE INNERVATION; NERVE BLOCK; NERVE DEGENERATION; NERVE ENDING; NEUROMUSCULAR SYNAPSE; NONHUMAN; PLANTARIS MUSCLE; PRIORITY JOURNAL; SCIATIC NERVE; SOLEUS MUSCLE; SYNAPTIC TRANSMISSION; WILD TYPE;

ANIMALS; DOGS; GLYCOLYSIS; MICE; MICE, TRANSGENIC; MOTOR NEURON DISEASE; MOTOR NEURONS; MUSCLE, SKELETAL; NEUROMUSCULAR JUNCTION; SUPEROXIDE DISMUTASE;

EID: 84864066028     PISSN: 09699961     EISSN: 1095953X     Source Type: Journal    
DOI: 10.1016/j.nbd.2012.06.017     Document Type: Article

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