Somatostatin Interneurons Promote Neuronal Synchrony in the Neonatal Hippocampus

Abstract

Summary: Synchronized activity is a universal characteristic of immature neural circuits that is essential for their developmental refinement and strongly depends on GABAergic neurotransmission. A major subpopulation of GABA-releasing interneurons (INs) expresses somatostatin (SOM) and proved critical for rhythm generation in adulthood. Here, we report a mechanism whereby SOM INs promote neuronal synchrony in the neonatal CA1 region. Combining imaging and electrophysiological approaches, we demonstrate that SOM INs and pyramidal cells (PCs) coactivate during spontaneous activity. Bidirectional optogenetic manipulations reveal excitatory GABAergic outputs to PCs that evoke correlated network events in an NKCC1-dependent manner and contribute to spontaneous synchrony. Using a dynamic systems modeling approach, we show that SOM INs affect network dynamics through a modulation of network instability and amplification threshold. Our study identifies a network function of SOM INs with implications for the activity-dependent construction of developing brain circuits. : Developing neural circuits generate burst-like spontaneous activity. Flossmann et al. report a mechanism whereby somatostatin interneurons promote neuronal synchrony in the neonatal hippocampus. This action depends on depolarizing GABAergic output synapses and requires chloride uptake via NKCC1. Their findings have implications for the activity-dependent refinement of developing brain circuits. Keywords: GABA, interneurons, development, hippocampus, optogenetics