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      Oxytocin Enhances Social Recognition by Modulating Cortical Control of Early Olfactory Processing

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          SUMMARY

          Oxytocin promotes social interactions and recognition of conspecifics that rely on olfaction in most species. The circuit mechanisms through which oxytocin modifies olfactory processing are incompletely understood. Here, we observed that optogenetically induced oxytocin release enhanced olfactory exploration and same-sex recognition of adult rats. Consistent with oxytocin’s function in the anterior olfactory cortex, particularly in social cue processing, region-selective receptor deletion impaired social recognition but left odor discrimination and recognition intact outside a social context. Oxytocin transiently increased the drive of the anterior olfactory cortex projecting to olfactory bulb interneurons. Cortical top-down recruitment of interneurons dynamically enhanced the inhibitory input to olfactory bulb projection neurons and increased the signal-to-noise of their output. In summary, oxytocin generates states for optimized information extraction in an early cortical top-down network that is required for social interactions with potential implications for sensory processing deficits in autism spectrum disorders.

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          Author and article information

          Journal
          8809320
          1600
          Neuron
          Neuron
          Neuron
          0896-6273
          1097-4199
          21 April 2016
          21 April 2016
          4 May 2016
          04 May 2017
          : 90
          : 3
          : 609-621
          Affiliations
          [1 ]Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, 68159 Mannheim, Germany
          [2 ]Skirball Institute for Biomolecular Medicine, New York University School of Medicine, New York, NY 10016, USA
          [3 ]German Cancer Research Center, 69120 Heidelberg, Germany
          [4 ]Section on Neural Gene Expression, National Institute of Mental Health, NIH, Bethesda, MD 20892, USA
          [5 ]Sagol Department of Neurobiology, University of Haifa, Haifa 3498838, Israel
          Author notes
          [6]

          Present address: Institute of Neuroscience, University of Oregon, Eugene, OR 97403, USA

          Article
          PMC4860033 PMC4860033 4860033 nihpa774666
          10.1016/j.neuron.2016.03.033
          4860033
          27112498
          8c10622f-7020-4311-9208-2740e86a84f4
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