In the mammalian CNS, GABAB receptors mediate slow pre- and postsynaptic inhibition. Using extracellular recording from area CA3 of adult rat hippocampal slices and we have investigated the role of synaptic GABAB receptors in regulating kainate-induced subthreshold neuronal network oscillations in the gamma frequency range (25-80 Hz; mean frequency 30.9 ± 1.1 Hz; n=6). The GABAB receptor agonist baclofen largely eliminated gamma oscillations (n=3). The GABAB receptor antagonist, CGP55845, reversed this action of baclofen, but alone did not alter the power or frequency of ongoing oscillations. Thus, following addition of CGP55845 (1 µM), the power of kainate-driven gamma oscillations was 2.14 ± 0.81 µV2 cf. a baseline power of 1.72 ± 0.64 µV2, whilst the frequency was 29.2 ± 1.0 Hz (P>0.05, n=6). To examine the role of synaptically released GABA on network activity, we electrically stimulated stratum radiatum of CA3, whilst recording gamma oscillations from stratum pyramidale. Single stimuli produced a pronounced, transient (up to 1 s in duration), inhibition of gamma frequency oscillations. The gamma oscillations which re-emerged 300-500 ms after synaptic stimulation had a significantly slower period than those prior to stimulation (34.6 ± 1.4 Hz after stimulation cf. 38.0 ± 1.8 Hz prior to stimulation; P<0.01, n=13). This slowing of the gamma oscillations was transient, such that 4 s after stimulation, the gamma period had returned to baseline levels (37.3 ± 2.1 Hz; P=0.45, n=13). The stimulus-induced shutdown of network activity was significantly enhanced by the GABA uptake inhibitor tiagabine and largely inhibited by CGP55845. Multiple stimuli delivered at frequencies of 1-3 Hz resulted in an activity-dependent fatigue of the inhibition of gamma activity, such that, after a number of stimuli, oscillations could be detected tens of milliseconds after the stimulus. Interestingly, this activity-dependent fatigue of inhibition uncovered a stimulus-dependent temporal entrainment of the gamma oscillations. Furthermore, the amount of repetitive synaptic input that was required to cause this entrainment was dramatically reduced by GABAB receptor antagonism such that it was evident within just a few stimuli. These data suggest that convergent afferent synaptic activity can alter the precise temporal arrangement of neuronal network activity. Furthermore, the flow of such information into a functioning neuronal network is highly regulated by GABAB-receptor-mediated synaptic inhibition.