Effects of morphine and haloperidol on the electrical activity of rat nigrostriatal neurons

Abstract

The action of opiates on electrical activity in nigrostriatal neurons was compared with the actions of known dopamine receptor agonists and antagonists in order to clarify the effects of opiates on postsynaptic dopamine receptors in the striatum. The systemic administration of either morphine or haloperidol increased the rate of spontaneous firing of neurons in substantia nigra. The injection of either drug directly into the caudate nucleus of the striatum also increased the firing rates of nigral neurons. The administration of the opiate antagonist, naloxone, blocked or reversed the action of systemically or locally applied morphine on firing rates, but not those of haloperidol. The dopamine receptor agonists, dopa and apomorphine, decreased the firing rate in nigral neurons and also reversed the stimulation of firing rates by morphine. The agonists were only partially successful in reversing the effects of haloperidol. The differences in the ability of naloxone and dopa to reverse the stimulated firing rates produced by morphine or haloperidol support the hypothesis that opiates do not act directly on the postsynaptic dopamine receptor in the striatum.