The release of inhibitory transmitters from CNS neurons can be modulated by ionotropic glutamate receptors that are present in the presynaptic terminals. In the cerebellum, glutamate released from climbing fibres (but not from parallel fibres) activates presynaptic AMPA receptors and suppresses the release of the inhibitory transmitter, GABA, from basket cells onto post-synaptic Purkinje cells. This input specific modulation has been attributed to the close proximity of the climbing fibres to the axons of the basket cells. Our recent work indicates that glutamate released from parallel fibres can "spillover" and reach the axons of stellate cells. Here I test the possibility that this spillover glutamate can activate presynaptic AMPARs in stellate cells and in this way modulate their release of GABA. I find that stimulation of parallel fibres activates AMPA receptors and transiently suppresses autoreceptor and autaptic GABAergic currents in stellate cells. Activation of AMPA receptors reduces the release of GABA and the suppression occurs more frequently in immature cells that have a high release probability. By contrast the release of GABA from mature stellate cells that have a low release probability is potentiated by the activation of NMDA-type glutamate receptors on presynaptic terminals. Thus during development, the glutamatergic modulation of GABA release switches from an AMPA receptor-mediated transient suppression to a NMDA receptor-induced lasting potentiation.