Although recent histological, behavioral and clinical studies suggest that serotonin (5-HT) plays significant roles in the control of pallidal activity, only little is known about the physiological action of 5-HT in the pallidum. Our recent unit recoding study in monkeys suggested that 5-HT provides both presynaptic and postsynaptic modulations of pallidal neurons. The present study using rat brain slice preparations further explored these presynaptic and postsynaptic actions of 5-HT. Bath application of 5-HT or the 5-HT_1A/1B/1D/5/7 receptor (R) agonist 5-carboxamidotryptamine maleate (5-CT) depolarized some and hyperpolarized other pallidal neurons. Pretreatments of slices with blockers of the hyperpolarization-cyclic nucleotide activated current or with the 5-HT_2/7R selective antagonist mesulergine occluded 5-CT-induced depolarization. The 5-HT_1AR selective blocker N-[2-[4-(2-Methoxyphenyl)-1-piperazinyl]ethyl]-N-2-pyridinylcyclohexanecarboxamide maleate occluded the 5-CT induced hyperpolarization. These results suggested involvement of 5-HT₇R and 5-HT_1AR in the postsynaptic depolarization and hyperpolarization, respectively. 5-CT presynaptically suppressed both internal capsule stimulation-induced EPSCs and striatal stimulation-induced IPSCs. The potencies of 5-CT on the presynaptic effects were 20-25 times higher than on postsynaptic effects, suggesting that 5-HT mainly modulates presynaptic sites in the globus pallidus. Experiments with several antagonists suggested involvement of 5-HT_1B/DR in the presynaptic suppression of EPSCs. However, the receptor type involved in the presynaptic suppression of IPSCs was inconclusive. The present results provided evidence that 5-HT exerts significant control over the synaptic inputs and the autonomous activity of pallidal neurons.