The contribution of autophosphorylated alpha-calcium-calmodulin kinase II to injury-induced persistent pain

Neuroscience

Volumn 128, Issue 4, 2004, Pages 889-898

  Zeitz, K P ^a,c   Giese, K P ^b   Silva, A J ^b   Basbaum, A I ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

^b Univ C   (United States)

^c ELAN PHARMACEUTICALS   (United States)

Author keywords

formalin; mouse; second messengers

Indexed keywords

ALANINE; CALCIUM; CALMODULIN; PROTEIN FOS; PROTEIN KINASE (CALCIUM,CALMODULIN) II; THREONINE;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; AUTOPHOSPHORYLATION; CONTROLLED STUDY; EVOKED RESPONSE; IMMUNOFLUORESCENCE; IMMUNOREACTIVITY; INFLAMMATION; NERVE INJURY; NOCICEPTION; NOCICEPTIVE STIMULATION; NONHUMAN; PAIN; PAIN THRESHOLD; POINT MUTATION; PRIORITY JOURNAL; PROTEIN EXPRESSION; PROTEIN FUNCTION; SENSORY NERVE; SPINAL CORD DORSAL HORN; WILD TYPE;

ANIMALS; BEHAVIOR, ANIMAL; CA(2+)-CALMODULIN DEPENDENT PROTEIN KINASE; CALCIUM; CELL COUNT; EDEMA; FREUND'S ADJUVANT; GANGLIA, SPINAL; GLYCOPROTEINS; IMMUNOHISTOCHEMISTRY; INTERMEDIATE FILAMENT PROTEINS; MEMBRANE GLYCOPROTEINS; MICE; MICE, INBRED C57BL; MICE, MUTANT STRAINS; NERVE TISSUE PROTEINS; NOCICEPTORS; ONCOGENE PROTEINS V-FOS; PAIN; PAIN MEASUREMENT; PAIN THRESHOLD; PHOSPHORYLATION; PHYSICAL STIMULATION; PROTEIN KINASE C; REACTION TIME; SUBSTANCE P; TIME FACTORS; TRIGEMINAL GANGLION; WOUNDS AND INJURIES;

EID: 4644248924     PISSN: 03064522     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.neuroscience.2004.07.029     Document Type: Article

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