Selective disruption of the mammalian secretory apparatus enhances or eliminates calcium current modulation in nerve endings

Proceedings of the National Academy of Sciences of the United States of America

Volumn 105, Issue 17, 2008, Pages 6427-6432

  Silinsky, Eugene M ^a  

^a NORTHWESTERN UNIVERSITY   (United States)

Author keywords

Adenosine; Neuromuscular junction; Neurotransmitter release; Synaptic vesicles

Indexed keywords

ADENOSINE A1 RECEPTOR; BOTULINUM TOXIN; CALCIUM; RAB PROTEIN; SNARE PROTEIN; SYNAPTOBREVIN; SYNAPTOSOMAL ASSOCIATED PROTEIN 25; SYNTAXIN; ADENOSINE; CALCIUM CHANNEL;

ANIMAL EXPERIMENT; ARTICLE; CALCIUM CURRENT; CELL MEMBRANE; CONTROLLED STUDY; MOTOR NERVE; MOUSE; NERVE ENDING; NONHUMAN; PRIORITY JOURNAL; SYNAPSE VESICLE; ANIMAL; BIOLOGICAL MODEL; CHANNEL GATING; DRUG EFFECT; GENETICS; METABOLISM; MUTATION; SECRETORY VESICLE;

MAMMALIA;

ADENOSINE; ANIMALS; BOTULINUM TOXINS; CALCIUM CHANNELS; ION CHANNEL GATING; MICE; MODELS, BIOLOGICAL; MUTATION; NERVE ENDINGS; QA-SNARE PROTEINS; R-SNARE PROTEINS; RAB3A GTP-BINDING PROTEIN; SECRETORY VESICLES; SNARE PROTEINS; SYNAPTOSOMAL-ASSOCIATED PROTEIN 25;

EID: 44049100326     PISSN: 00278424     EISSN: 10916490     Source Type: Journal    
DOI: 10.1073/pnas.0708814105     Document Type: Article

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