Nociceptor-specific gene deletion reveals a major role for Nav 1.7 (PN1) in acute and inflammatory pain

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

Volumn 101, Issue 34, 2004, Pages 12706-12711

  Nassar, Mohammed A ^a   Stirling, L Caroline ^a   Forlani, Greta ^a   Baker, Mark D ^a   Matthewst, Elizabeth A ^a   Dickenson, Anthony H ^a   Wood, John N ^a  

^a UNIVERSITY COLLEGE LONDON   (United Kingdom)

Author keywords

[No Author keywords available]

Indexed keywords

RECOMBINASE; VOLTAGE GATED SODIUM CHANNEL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CONTROLLED STUDY; CYCLIC AMP RESPONSIVE ELEMENT; EDEMA; ERYTHEMA; ERYTHROMELALGIA; EXON; GENE DELETION; GENE EXPRESSION; GENE MAPPING; HEAT; INFLAMMATION; KNOCKOUT GENE; KNOCKOUT MOUSE; MAMMAL; MOUSE; MUSCLE; MYALGIA; NERVE; NERVE CELL; NEUROPATHOLOGY; NOCICEPTIVE RECEPTOR; NONHUMAN; NULL ALLELE; PAIN; PRIORITY JOURNAL;

ANIMALS; BEHAVIOR, ANIMAL; GENE DELETION; HUMANS; INFLAMMATION; MICE; MICE, KNOCKOUT; MICE, TRANSGENIC; NEURONS, AFFERENT; NEUROPEPTIDES; NOCICEPTORS; PAIN; PAIN MEASUREMENT; PATCH-CLAMP TECHNIQUES; SODIUM CHANNELS;

ANIMALIA; MAMMALIA;

EID: 4344670206     PISSN: 00278424     EISSN: None     Source Type: Journal    
DOI: 10.1073/pnas.0404915101     Document Type: Article

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