Continuous cold water swim produces analgesia that is partially mediated by a noradrenergic mechanism, but is independent of both serotonergic and opioid systems. On the other hand, intermittent cold water swim elicits analgesia which is partly mediated by an opioid mechanism; the contribution of the monoamines to the production of this analgesia is not known. Therefore, the present study was done to determine whether intermittent cold water swim is also mediated by noradrenergic and/or serotonergic substrates. Prior to either continuous (3.5 min) or intermittent (10 sec in, 10 sec out for 6 min) cold water (4 degrees C) swim, male Sprague-Dawley rats (225-250 g) were administered either the noradrenergic receptor blocker phentolamine (30 micrograms), the serotonergic blocker methysergide (30 micrograms) or artificial cerebrospinal fluid to the fifth lumbar vertebral spinal level via chronic intrathecal catheters. Phentolamine significantly attenuated the analgesia resulting from both continuous and intermittent cold water swim. Methysergide attenuated intermittent cold water swim analgesia, but was without effect on continuous cold water swim analgesia. Phentolamine, but not methysergide, also attenuated continuous footshock- (2.5 mA for 3 min) induced analgesia. The similarity between the effects of phentolamine and methysergide on continuous footshock and continuous cold water swim analgesia suggests that the effects of these drugs on cold water swim analgesia are not attributable to changes in thermoregulation. These results suggest that a spinal noradrenergic mechanism is involved in the mediation of both forms of cold water swim analgesia, whereas a spinal serotonergic mechanism is involved in only intermittent cold water swim analgesia.