title: The effect of gabapentin and ketorolac on allodynia and conditioned place preference in antibody-induced inflammation.
abstract: Glucose-6-phosphate isomerase and collagen type II antibody-induced arthritis models (K/BxN and CAIA, respectively) have an inflammatory and a post-inflammatory phase. Both phases display robust tactile allodynia. In previous work, inflammatory phase allodynia was reversed by gabapentin and ketorolac, whereas in late phase only gabapentin was effective. Here, we sought to determine if the effects of these two drugs during the early and late phases of the two arthritis models were observed in the conditioned place preference (CPP) paradigm, indicating a differential drug effect on the aversive state.
  
  
  
  Male C57BL/6 mice received K/BxN serum intraperitoneally, while male BALB/c mice received collagen type II antibody cocktail intravenously. After onset of inflammation and allodynia, we assessed effects of i.p. gabapentin (100 mg/kg) or ketorolac (15 mg/kg) using a CPP paradigm: 2 days adaptation, 2 days conditioning (vehicle in morning and drug in afternoon), preference testing on day 5.
  
  
  
  Consistent with the effects upon allodynia, both gabapentin and ketorolac produced a preference for the drug-paired compartment in the early phase of the K/BxN model, while gabapentin, but not ketorolac, resulted in a place preference during late phase. In the CAIA model, consistent with differential effects upon allodynia, gabapentin produced a preference in the early phase and a trend in the late phase, whereas ketorolac was ineffective at either time.
  
  
  
  CPP validated the aversive state in the inflammatory and post-inflammatory phases of the K/BxN and CAIA arthritis models and correspondence between the anti-hyperpathic pharmacology as defined by thresholds and CPP.
authors.affiliation: Department of Anesthesiology, University of California San Diego, USA.|Department of Anesthesiology and Pain Medicine, College of Medicine, The Catholic University of Korea, South Korea.
authors.forename: H J
authors.initials: HJ
authors.lastname: Park
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institutet, Sweden.
authors.forename: K
authors.initials: K
authors.lastname: Sandor
authors.affiliation: Department of Anesthesiology, University of California San Diego, USA.|Department of Physiology and Pharmacology, Karolinska Institutet, Sweden.
authors.forename: J
authors.initials: J
authors.lastname: McQueen
authors.affiliation: Department of Anesthesiology, University of California San Diego, USA.|Department of Medicine, University of California San Diego, USA.
authors.forename: S A
authors.initials: SA
authors.lastname: Woller
authors.affiliation: Department of Physiology and Pharmacology, Karolinska Institutet, Sweden.
authors.forename: C I
authors.initials: CI
authors.lastname: Svensson
authors.affiliation: Department of Medicine, University of California San Diego, USA.
authors.forename: M
authors.initials: M
authors.lastname: Corr
authors.affiliation: Department of Anesthesiology, University of California San Diego, USA.
authors.forename: T L
authors.initials: TL
authors.lastname: Yaksh
mesh_terms: D000588:Amines / Q000627:therapeutic use*; D000700:Analgesics / Q000627:therapeutic use*; D000818:Animals; D001168:Arthritis / Q000188:drug therapy* / Q000209:etiology; D003509:Cyclohexanecarboxylic Acids / Q000627:therapeutic use*; D004195:Disease Models, Animal; D000077206:Gabapentin; D005956:Glucose-6-Phosphate Isomerase; D006930:Hyperalgesia / Q000188:drug therapy*; D020910:Ketorolac / Q000627:therapeutic use*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D005680:gamma-Aminobutyric Acid / Q000627:therapeutic use*
chemical_list: D000588:Amines; D000700:Analgesics; D003509:Cyclohexanecarboxylic Acids; D005680:gamma-Aminobutyric Acid; D000077206:Gabapentin; D005956:Glucose-6-Phosphate Isomerase; D020910:Ketorolac