Astrocyte-mediated potentiation of inhibitory synaptic transmission

We investigated the role of astrocytes in activity-dependent modulation of inhibitory synaptic transmission in hippocampal slices. Repetitive firing o f an interneuron decreased the probability of synaptic failures in spike-ev oked inhibitory postsynaptic currents (unitary IPSCs) in CA1 pyramidal neur ons. The GABA(B)-receptor antagonist CCP55845A abolished this effect. Direc t stimulation of astrocytes, or application of the GABA(B)-receptor agonist baclofen, potentiated miniature inhibitory postsynaptic currents (mIPSCs) in pyramidal neurons. These effects were blocked by inhibition of astrocyti c calcium signaling with the calcium chelator BAPTA or by antagonists of th e ionotropic glutamate receptors. These observations suggest that interneur onal firing elicits a GABA(B)-receptor-mediated elevation of calcium in sur rounding astrocytes, which in turn potentiates inhibitory transmission. Ast rocytes may therefore be a necessary intermediary in activity-dependent mod ulation of inhibitory synapses in the hippocampus.