A comparison of the neurochemicals effects of buprenorphine with those of morphine and haloperidol in rats

Abstract

The effect of a wide range of doses of buprenorphine (0.001–10 mg·kg −1, s.c.), a partial agonist at mu (μ) oipiate receptors, was studied on (a) the steady state levels of dopamine, noradrenaline, 5-hydroxytryptamine, homovanillic acid, 3-methyoxy-4-hydroxyphenylglycol and 5-hydroxyindole acetic acid and (b) the levels of dopamine and noradrenaline in rat brain following treatment with α-MpT. Morphine (1–30 mg·kg −1) and haloperidol (0.01–3 mg·kg −1) were used as reference agents. Buprenorphine increased the α-MpT-induced rate of dopamine depletion but had no significant effect on that of noradrenaline. Similar results were obtained with morphine except that the highest dose of morphine tested (30 mg·kg −) increased the α-MpT-induced depletion of noradrenaline. The apparently similar effects of buprenorphine and haloperidol on dopaminergic neurotransmission were distingused by pretreating the rats with naloxone. Thus, naloxone antagonized the increased in homovanillic acid caused by nuprenorphine but not that caused by haloperidol; also, naloxone antagonized the increased rate of α-MpT-induced dopamine depletion associated with buprenorphine but not that associated with haloperidol. These neurochemical results, when combined with data from pervious behavioural studies, support the view that one site of action of buprenorphine is on opiate receptors located presynaptically on dopaminergic neurones.