title: Effects of opioid receptor activation on thermal antinociception in red-eared slider turtles (Trachemys scripta).
abstract: OBJECTIVE
  To determine the effects of mu-, delta-, and kappa-opioid receptor (MOR, DOR, and KOR, respectively) activation on thermal antinociception in red-eared slider turtles Trachemys scripta.
  
  
  METHODS
  51 adult turtles.
  
  
  METHODS
  Infrared heat stimuli were applied to the plantar surface of turtle hind limbs. Thermal hind limb withdrawal latencies (HLWLs) were measured before (baseline) and at intervals after SC administration of various doses of saline (0.9% NaCl) solution (SS), MOR, DOR, or KOR agonists (3 to 13 turtles/treatment). Treatment with a DOR antagonist SC prior to DOR agonist administration was also evaluated.
  
  
  RESULTS
  Treatment with an MOR agonist ([D-Ala(2), N-Me-Phe(4), Gly(5)-ol]-enkephalin acetate salt [DAMGO; 1.3 or 6.6 mg/kg]) increased HLWLs (from baseline) at 2 to 8 hours after injection; at the higher dose, the maximum mean increase was 5.6 seconds at 4 hours. Treatment with a DOR agonist ([D-Ala(2), D-Leu(5)]-enkephalin acetate salt [DADLE; 25 mg/kg]) increased mean HLWL by 11.3 seconds at 4 hours; however, treatment with DADLE (5.8 mg/kg) or with another DOR agonist ([D-Pen(2),(5)]-enkephalin hydrate [DPDPE; 1.2 or 6.3 mg/kg]) did not alter HLWL, compared with SS effects. Administration of a DOR antagonist (naltrindole hydrochloride; 10 mg/kg) prior to DADLE administration (25 mg/kg) increased mean HLWL by 2.7 seconds at 4 hours. One KOR agonist, U50488 ([-]-trans-[1S,2S]-U50488 hydrochloride hydrate; 6.7 mg/kg) decreased HLWL steadily from 2 to 24 hours (less than baseline value); another KOR agonist, U69593 ([+]-[5alpha,7alpha,8beta]-N-Methyl-N-[7-{1-pyrrolidinyl}-1-oxaspiro{4.5}dec-8-yl]-benzene-acet-amide; 6.7 or 26 mg/kg) did not alter HLWLs, compared with SS effects.
  
  
  CONCLUSIONS
  Opioid-dependent thermal antinociception in turtles appeared to be attributable mainly to MOR activation with a relatively minor contribution of DOR activation.
authors.affiliation: Department of Surgical Sciences, Center for Global Health, School of Veterinary Medicine and Public Health, University of Wisconsin, Madison, WI 53706, USA.
authors.forename: Kurt K
authors.initials: KK
authors.lastname: Sladky
authors.forename: Matthew E
authors.initials: ME
authors.lastname: Kinney
authors.forename: Stephen M
authors.initials: SM
authors.lastname: Johnson
mesh_terms: D000701:Analgesics, Opioid / Q000494:pharmacology; D000818:Animals; D044482:Benzeneacetamides / Q000494:pharmacology; D018592:Cross-Over Studies; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)- / Q000494:pharmacology*; D020881:Enkephalin, D-Penicillamine (2,5)- / Q000494:pharmacology*; D016308:Enkephalin, Leucine-2-Alanine / Q000494:pharmacology; D005260:Female; D006358:Hot Temperature; D008297:Male; D009619:Nociceptors; D011759:Pyrrolidines / Q000494:pharmacology; D017450:Receptors, Opioid, mu / Q000187:drug effects / Q000502:physiology*; D012965:Sodium Chloride / Q000494:pharmacology*; D014426:Turtles / Q000502:physiology*
chemical_list: D000701:Analgesics, Opioid; D044482:Benzeneacetamides; D011759:Pyrrolidines; D017450:Receptors, Opioid, mu; D020875:Enkephalin, Ala(2)-MePhe(4)-Gly(5)-; D012965:Sodium Chloride; D016308:Enkephalin, Leucine-2-Alanine; D020881:Enkephalin, D-Penicillamine (2,5)-; C045444:U 69593