ABSTRACT
Aim To investigate the effects of L-type calcium channel blockers on tramadol-induced analgesia.Methods Hot-plate test and writhing test were used to measure the analgesia induced by tramadol. Verapamil, nimodipine or nifedipine was co-administrated with tramadol to determine its effects on tramadol analgesia.Results Tramadol (10, 20, 40 mg?kg -1 in hot-plate test or 2, 5,10 mg?kg -1 in writhing test) produced significantly analgesia in hot-plate test and writhing test. Co-administration of verapamil and tramadol prolonged the latency of pain response of mice in hot-plate test.In writhing test, verapamil, nimodipine and nifedipine could potentiate the analgesic effect of tramadol in a dose-dependent manner.Conclusion L-type calcium channel blockers can potentiate tramadol-induced analgesia. Calcium influx mediated by L-type calcium channels may be involved in tramadol-induced analgesia.
ABSTRACT
AIM To investigate the effects of trifluoperazine on naloxone precipitated withdrawal symptoms in morphine dependent rats and mice, and its pharmacological mechanisms. METHODS\ Naloxone precipitated tests in morphine dependent rats and mice were used. RESULTS\ Trifluoperazine(2～20 mg?kg -1 ) dose dependently inhibited naloxone precipitated withdrawal jumping, wet dog shakes, paw tremor and weight loss in morphine dependent mice. With ip trifluoperazine (5～20 mg?kg -1 ), most of positive withdrawal symptoms, including jumping, wet dog shakes, defeacation, weight loss, teeth chattering, salivation, diarrhea, ptosis and irritating, induced by naloxone in morphine dependent rats were significantly reduced. Apomorphine (2～8 mg?kg -1 ), a mixed DA 1/DA 2 receptor agonist, did not affect inhibition of trifluoperazine on naloxone precipitated withdrawal symptoms in morphine dependent mice. However, nifedipine(5～20 mg?kg -1 ), a L type voltage sensitive calcium channel blocker, enhanced a pharmacological action of trifluoperazine against naloxone precipitated symptoms in morphine dependent mice. CONCLUSION\ Trifluoperazine attenuates naloxone precipitated withdrawal symptoms in morphine dependent rats and mice by inhibiting the activity of post receptor calmodulin, but it does not antagonizes DA 2 receptor, in central nervous system.