Yohimbine potentiates cold-water swim analgesia: re-evaluation of a noradrenergic role.

Continuous cold-water swims (CCWS) elicit a nonopioid and neurohormonal analgesia which displays adaptation. The norepinephrine (NE) system has been implicated since parallel alterations in NE occur following acute and repeated CCWS exposure, and since CCWS analgesia is reduced by locus coeruleus lesions and is potentiated by clonidine and desipramine. The present study evaluated the effects of the alpha-2 NE receptor antagonist, yohimbine upon CCWS (2 degrees C for 3.5 min) analgesia on the jump and tail-flick tests, CCWS hypothermia, and basal nociceptive and thermoregulatory measures in rats. Yohimbine (0.1-2.0 mg/kg, IP) dose-dependently increased basal jump thresholds and potentiated CCWS analgesia: these effects appeared to be additive. Yohimbine potentiated CCWS analgesia on the tail-flick test without altering basal latencies. Yohimbine failed to alter either CCWS hypothermia or basal thermoregulation. Since yohimbine and clonidine, an alpha-2 NE receptor antagonist and agonist respectively, similarly potentiate CCWS analgesia, it appears that NE effects are orthoganol to the intrinsic system mediating CCWS.