Role of NK-1 neurotransmission in opioid-induced hyperalgesia

Pain

Volumn 116, Issue 3, 2005, Pages 276-288

  King, Tamara ^a   Gardell, Luis R ^a   Wang, Ruizhong ^a   Vardanyan, Anna ^a   Ossipov, Michael H ^a   Philip Malan Jr , T ^a   Vanderah, Todd W ^a   Hunt, Stephen P ^b   Hruby, Victor J ^c   Lai, Josephine ^a   Porreca, Frank ^a  

^a UNIVERSITY OF ARIZONA COLLEGE OF MEDICINE   (United States)

^b UNIVERSITY COLLEGE LONDON   (United Kingdom)

^c University of Arizona   (United States)

Author keywords

Inflammatory pain; NK 1 receptor; Opioid induced hyperalgesia; Substance P

Indexed keywords

CAPSAICIN; MORPHINE; NK 1 RECEPTOR; OPIATE; RECEPTOR; SUBSTANCE P; UNCLASSIFIED DRUG;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; HYPERALGESIA; INTERNALIZATION; MALE; NEUROCHEMISTRY; NEUROTRANSMISSION; NOCICEPTIVE STIMULATION; NONHUMAN; PAIN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RAT; SPINAL CORD DORSAL HORN; WILD TYPE;

ANIMALS; CELL COUNT; DRUG INTERACTIONS; HEAT; HYPERALGESIA; IMMUNOHISTOCHEMISTRY; MALE; MICE; MICE, KNOCKOUT; MORPHINE; NARCOTICS; PAIN MEASUREMENT; PROTEIN TRANSPORT; RATS; RATS, SPRAGUE-DAWLEY; REACTION TIME; RECEPTORS, NEUROKININ-1; SPINAL CORD; SUBSTANCE P; SYNAPTIC TRANSMISSION; TIME FACTORS; TOUCH; TRYPTOPHAN;

EID: 21844474563     PISSN: 03043959     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.pain.2005.04.014     Document Type: Article

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