Color code indicates the frequency of the detected events. (C) Superimposition of all network events detected during a 5-min baseline recording (left) and after oxytocin application (right). (B) Traces show fluorescent changes in V1 and S1 before and after oxytocin application. (Right) Network events after oxytocin (Oxt) application are shown. (Left) Single-frame images depict network events activating V1 and/or S1 during baseline recordings before oxytocin application. Oxytocin Affects Spontaneous Network Events Differentially across Sensory Cortices (A) Wide-field calcium imaging of spontaneous activity in V1 and S1 before eye opening. Thus, oxytocin decreases the excitatory/inhibitory (E/I) ratio by recruiting SST + interneurons and modulates specific features of V1 spontaneous activity patterns that are crucial for the wiring and refining of developing sensory circuits.Ĭalcium imaging mouse neuromodulator neuronal excitability patch-clamp somatosensory cortex.Ĭopyright © 2020 The Author(s). Accordingly, pharmacogenetic silencing of V1 SST + interneurons fully blocked oxytocin's effect on inhibition in vitro as well its effect on spontaneous activity patterns in vivo. Somatostatin-positive (SST +) interneurons expressed the oxytocin receptor and were activated by oxytocin in V1. Patch-clamp recordings in slices and RNAscope showed that oxytocin affects S1 excitatory and inhibitory neurons similarly, whereas in V1, oxytocin targets only inhibitory neurons. In vivo, oxytocin strongly decreased the frequency and pairwise correlations of spontaneous activity events in the primary visual cortex (V1), but it did not affect the frequency of spontaneous network events in the somatosensory cortex (S1). Here, we report that the neuromodulator oxytocin differentially shapes spontaneous activity patterns across sensory cortices. However, how neuromodulation influences this activity is not fully understood. Electronic address: network activity shapes emerging neuronal circuits during early brain development prior to sensory perception. Electronic address: 6 Department of Synapse and Network Development, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands Department of Functional Genomics, Center for Neurogenomics and Cognitive Research, VU University Amsterdam, 1081 HV Amsterdam, the Netherlands. Electronic address: 5 Max Planck Institute for Brain Research, Computation in Neural Circuits, 60438 Frankfurt am Main, Germany TUM School of Life Sciences, Technical University of Munich, 85354 Freising, Germany. Electronic address: 4 Program in Neuroscience, The Florida State University, Tallahassee, FL 32306, USA Department of Psychology, The Florida State University, Tallahassee, FL 32306, USA. Electronic address: 3 Max Planck Institute for Brain Research, Computation in Neural Circuits, 60438 Frankfurt am Main, Germany TUM School of Life Sciences, Technical University of Munich, 85354 Freising, Germany. Electronic address: 2 Department of Synapse and Network Development, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands. 1 Department of Synapse and Network Development, Netherlands Institute for Neuroscience, 1105 BA Amsterdam, the Netherlands.
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