title: Suckling and sucrose ingestion suppress persistent hyperalgesia and spinal Fos expression after forepaw inflammation in infant rats.
abstract: Sweet taste and nonnutritive suckling produce analgesia to transient noxious stimuli in infant rats and humans. The present study evaluated the pain-modulating effects of sucrose and suckling in a rat model of persistent pain and hyperalgesia that mimics the response to tissue injury in humans. Fore- and hindpaw withdrawal latencies from a 30 degrees or 48 degrees C brass stylus were determined in 10-day-old rats following paw inflammation induced by complete Freund's adjuvant (CFA; 1:1 injected s.c. in a 0.01 ml volume). CFA markedly decreased escape latencies to both 48 degrees and 30 degrees C stimulation, thereby demonstrating thermal hyperalgesia and mechanical allodynia. The combination of nonnutritive suckling and sucrose (7.5%, 0.01-0.06 ml/min) infusion markedly increased escape latencies to forepaw stimulation in both CFA-treated and control rats. In contrast, intraoral sucrose and suckling did not increase hindpaw withdrawal latencies in either control or CFA-inflamed rats. The effect was specific to sweet taste because neither water nor isotonic saline infusion affected forepaw escape latencies. Parallel findings were obtained for CFA-induced Fos-like immunoreactivity (Fos-LI), a marker of neuronal activation. Fos-LI was selectively induced in cervical and lumbar regions ipsilateral to forepaw and hindpaw inflammation, respectively. Suckling-sucrose treatment significantly reduced Fos-LI at the cervical but not at the lumbar regions. These findings demonstrate: (i) the development of persistent pain and hyperalgesia in 10-day-old rats that can be attenuated by endogenous pain-modulating systems activated by taste and nonnutritive suckling; (ii) the mediation of the sucrose-suckling analgesia and antihyperalgesia at the spinal level; and (iii) a differential rostrocaudal maturation of descending pain-modulating systems to the spinal cord of 10-day-old rats. These findings may provide new clinical approaches for engaging endogenous analgesic mechanisms in infants following tissue injury and inflammation.
authors.affiliation: Department of Oral and Craniofacial Biological Sciences, University of Maryland Dental School, Baltimore 21201, USA. knr001@dental3.ab.umd.edu
authors.forename: K
authors.initials: K
authors.lastname: Ren
authors.forename: E M
authors.initials: EM
authors.lastname: Blass
authors.forename: Q
authors.initials: Q
authors.lastname: Zhou
authors.forename: R
authors.initials: R
authors.lastname: Dubner
mesh_terms: D000818:Animals; D000833:Animals, Suckling; D004435:Eating / Q000502:physiology*; D005069:Evaluation Studies as Topic; D005260:Female; D005552:Forelimb / Q000473:pathology; D006930:Hyperalgesia / Q000628:therapy*; D007249:Inflammation; D007774:Lactation / Q000502:physiology; D008297:Male; D010146:Pain / Q000378:metabolism*; D010812:Physical Stimulation; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D011930:Reaction Time; D013116:Spinal Cord / Q000378:metabolism*; D013395:Sucrose / Q000627:therapeutic use; D013549:Sweetening Agents / Q000627:therapeutic use; D013649:Taste; D014110:Touch / Q000502:physiology*
chemical_list: D016760:Proto-Oncogene Proteins c-fos; D013549:Sweetening Agents; D013395:Sucrose