Astrocytes control GABAergic inhibition of neurons in the mouse barrel cortex

Non-technical summary  In the last few years astrocytes have come to be recognized as active elements contributing to brain activity. They sense and modulate neuronal activity, and often changes in their cytosolic Ca2+ are essential for neuron–glia interactions. In the present study we interfered with intracellular calcium signalling in astrocytes in mouse somatosensory cortex by dialysis with the calcium chelator BAPTA. Such treatment increased excitability of the nearby neurons. The effect of astrocytic calcium chelation was mimicked by pharmacological inhibition of GABA receptors, suggesting that this control is GABA mediated through a combined involvement of GABAA and GABAB receptors. This finding demonstrates a role for astrocytes in the regulation of neural inhibition in somatosensory (barrel) cortex and adds a new variant to the growing number of pathways by which astrocytes can modulate neuronal networks. Abstract  Astrocytes in the barrel cortex respond with a transient Ca2+ increase to neuronal stimulation and this response is restricted to the stimulated barrel field. In the present study we suppressed the astrocyte response by dialysing these cells with the Ca2+ chelator BAPTA. Electrical stimulation triggered a depolarization in stellate or pyramidal ‘regular spiking’ neurons from cortex layer 4 and 2/3 and this response was augmented in amplitude and duration after astrocytes were dialysed with BAPTA. Combined blockade of GABAA and GABAB receptors mimicked the effect of BAPTA dialysis, while glutamate receptor blockers had no effect. Moreover, the frequency of spontaneous postsynaptic currents was increased after BAPTA dialysis. Outside the range of BAPTA dialysis astrocytes responded with a Ca2+ increase, but in contrast to control, the response was no longer restricted to one barrel field. Our findings indicate that astrocytes control neuronal inhibition in the barrel cortex.