Highlights d Neonatal SOM interneurons establish excitatory GABAergic output synapses in CA1 d Spontaneous activity of SOM interneurons drives CA1 network synchrony d The synchronizing capacity of SOM interneurons depends on NKCC1 d GABA-mediated excitation modulates network instability and amplification threshold
A new mechanism involving intermediate gating states of calcium channels explains how analogue postsynaptic potentials influence neurotransmitter release.
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