In the central nervous system, the opioid and non-opioid transmitter system jointly compete with multiple pathophysiological processes. The in vitro neuronal model of rat (Wistar) caudate putamen and reverse transcription-poly-merase chain reaction were used to examine the effects of neurotensin and/or morphine on the expression of mu or delt-opioid receptor mRNA. In the present study neurotensin (10 nmol/l) promoted but morphine (0.001 mmol/l) reduced mu or delt-opioid receptor mRNA expression (n=4, P<0.01 or P<0.05) at 24 h after administration. Interestingly, when cells were incubated with neurotensin (10 nmol/l) plus morphine (0.001 mmol/l), the inhibition of mu or delt-opioid receptor by morphine was attenuated. A mouse tail reaction test was carried out to examine the effects of neurotensin on tail erection induced by morphine, and to investigate the effects of neurotensin on the morphine addictive ethnology. Sixty mice (Kunming, China, Female=30, Male=30, Body Weight=15.1±0.7 g) were used. Results showed that the mice were demonstrating tail erection, continual running and jumping, the behaviour was significantly altered within 2 hours after injection of morphine (15 mg/kg) compared with the normal saline control group, whose behaviour was unaltered and no tail erection was noted (n=10). However, after pre-treatment with neurotensin (0.1 mg/kg), 40 percent of such tail erection behaviours were reduced compared with the morphine-treated group. After a morphine injection in the mice pre-treated with neurotensin (0.3 mg/kg) no tail reaction was noted, and the mice were significantly less active. This study has provided experimental evidence to partially explain the mechanisms of neurotensin analgesia and neurotensin-enhanced acupuncture analgesia at the level of gene expression. Neurotensin at a higher concentration may inhibit the tail-erecting reaction induced by morphine, suggesting that it can partly antagonise the effects of morphine addiction, and this effect of neurotensin may be associated with its up-alterations in mu and/or delt-opioid receptor expression.