SUCKLING AND SUCROSE INGESTION SUPPRESS PERSISTENT HYPERALGESIA AND SPINAL FOS EXPRESSION AFTER FOREPAW INFLAMMATION IN INFANT RATS

Sweet taste and nonnutritive suckling produce analgesia to transient n oxious 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 in jury in humans, Fore- and hindpaw withdrawal latencies from a 30 degre es or 48 degrees C brass stylus were determined in 10-day-old rats fol lowing paw inflammation induced by complete Freund's adjuvant (CFA; 1: 1 injected s.c. in a 0.01 ml volume), CFA markedly decreased escape la tencies to both 48 degrees and 30 degrees C stimulation, thereby demon strating thermal hyperalgesia and mechanical allodynia, The combinatio n of nonnutritive suckling and sucrose (7.5%, 0.01-0.06 ml/min) infusi on markedly increased escape latencies to forepaw stimulation in bath CPA-treated and control rats, In contrast, intraoral sucrose and suckl ing did not increase hindpaw withdrawal latencies in either control or CFA-inflamed rats, The effect was specific to sweet taste because nei ther water nor isotonic saline infusion affected forepaw escape latenc ies, Parallel findings were obtained for CFA-induced Fos-like immunore activity (Fos-LI), a marker of neuronal activation, Fos-Li was selecti vely induced in cervical and lumbar regions ipsilateral to forepaw and hindpaw inflammation, respectively, Suckling-sucrose treatment signif icantly 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 antihyperalge sia at the spinal level; and (iii) a differential rostrocaudal maturat ion of descending pain-modulating systems to the spinal cord of 10-day -old rats, These findings may provide new clinical approaches for enga ging endogenous analgesic mechanisms in infants following tissue injur y and inflammation.