Short term plasticity is of great importance for the overall function of the neuronal network. Mechanisms intrinsic to the synapse such as vesicle depletion and residual calcium are well established mechanism mediating short-term plasticity. In addition, presynaptic terminals express receptors whose activation can modulate the release. We have recently described an astrocyte-mediated transient heterosynaptic depression (tHeSD) in the CA1, stratum radiatum of hippocampus. A 3-impulse 50 Hz conditioning burst produces a 25% reduction in release probability of neighbouring synapses within 500 ms in slices from 3 week old rats (Andersson et al, 2007). Here we have addressed the question to what extent the synapses providing the conditioning stimuli are affected by this transient depression. To examine this, a paired-pulse stimulus was applied 500 ms after the conditioning burst (3 impulses, 50 Hz) to the same (homosynaptic) synaptic input. Compared to the 1^st fEPSP in the conditioning 3-impulse burst, the 1^st fEPSP in the paired-pulse stimuli was depressed by 50 %. This transient homosynaptic depression (tHoSD) appeared to be mediated by astrocytes since it was completely blocked by the astrocyte-specific metabolic inhibitor fluoroacetate (FAC). Similar to the tHeSD, the tHoSD exhibited a clear developmental profile with only a 7% depression in slices from rats aging 6 to 11 postnatal days. In further agreement with the tHeSD, GABA_B and mGlu receptors were involved in the tHoSD. These results show that a short burst gives rise to a previously unrecognized form of short term plasticity - a synaptic auto-inhibition mediated by astrocytes.