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In rats, we have previously shown that inflammatory pain experienced on the day of birth significantly decreases adult somatosensory thresholds and responses to anxiety\u2010 and stress\u2010provoking stimuli. These long\u2010term changes in pain and stress responsiveness are accompanied by two\u2010fold increases in central met\u2010enkephalin and \u03b2\u2010endorphin expression. However, the time course over which these changes in central opioid peptide expression occur, relative to the time of injury, are not known. The present studies were conducted to determine whether the observed changes in adult opioid peptide expression were present within the first postnatal week following injury. The impact of neonatal inflammation on plasma corticosterone, a marker for stress reactivity, was also determined. Brain, spinal cord, and trunk blood were harvested at 24 h, 48 h, and 7 d following intraplantar administration of the inflammatory agent carrageenan on the day of birth. Radioimmunoassay was used to determine plasma corticosterone and met\u2010enkephalin and \u03b2\u2010endorphin levels within the forebrain, cortex, midbrain, and spinal cord. Within 24 h of injury, met\u2010enkephalin levels were significantly increased in the midbrain, but decreased in the spinal cord and cortex; forebrain \u03b2\u2010endorphin levels were significantly increased as a result of early life pain. Corticosterone levels were also significantly increased. At 7 d post\u2010injury, opioid peptides remained elevated relative to controls, suggesting a time point by which injury\u2010induced changes become programmed and permanent. \u00a9 2013 Wiley Periodicals, Inc. 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