The secretion of prolactin from the pituitary is negatively controlled by tuberoinfundibular dopamine (TIDA) neurones. The electrical properties of TIDA cells have recently been identified as a modulatory target of neurotransmitters and hormones in the lactotrophic axis. The role of the GABA(B) receptor in this control has received little attention, yet is of particular interest because it may act as a TIDA neurone autoreceptor. Here, this issue was explored in a spontaneously active rat TIDA in vitro slice preparation using whole-cell recordings. Application of the GABA(B) receptor agonist, baclofen, dose-dependently slowed down or abolished the network oscillations typical of this preparation. Pharmacological manipulations identify the underlying mechanism as an outward current mediated by G-protein-coupled inwardly rectifying K+-like channels. In addition to this postsynaptic modulation, we describe a presynaptic modulation where GABA(B) receptors restrain the release of glutamate and GABA onto TIDA neurones. Our data identify both pre- and postsynaptic modulation of TIDA neurones by GABA(B) receptors that may play a role in the neuronal network control of pituitary prolactin secretion and lactation.