In experiments on male Wistar rats, the acute phase reaction was induced by a bolus intravenous injection of Escherichia coli lipopolysaccharide (10 microg/kg) through a silicon catheter pre-implanted into the jugular vein. The colonic and skin temperature was measured with thermocouples. Changes in nociception were assessed based on tail flick latency (TFL) in response to a noxious heat stimulus. In this work, we observed the development of biphasic fever and phasic changes in TFL, namely, hyperalgesia in the first period of the acute phase reaction and hypoalgesia in its second phase. The catabolism of serotonin increased most considerably in the initial period of the acute phase reaction in the midbrain, striatum, and rostrodorsomedial medulla (on average, by 20-25%, 35-40%, and 95-100%, respectively). In the second phase of the acute phase reaction, despite a significant increase in the serotonin content in the striatum, midbrain, and cerebellum, there were no significant changes in serotonin catabolism in these parts of the CNS, which coincided with hypoalgesia. Thus, the phasic changes in TFL and colonic temperature after initiation of the acute phase reaction were accompanied by determinate changes in the catabolism of serotonin in different brain parts.