Transient oxytocin signaling primes the development and function of excitatory hippocampal neurons

Silvia Ripamonti, Mateusz C. Ambrozkiewicz, Francesca Guzzi, Marta Gravati, Gerardo Biella, Ingo Bormuth, Matthieu Hammer, Liam P. Tuffy, Albrecht Sigler, Hiroshi Kawabe, Katsuhiko Nishimori, Mauro Toselli, Nils Brose, Marco Parenti, Jeong Seop Rhee

    Research output: Contribution to journalArticlepeer-review

    38 Citations (Scopus)

    Abstract

    Beyond its role in parturition and lactation, oxytocin influences higher brain processes that control social behavior of mammals, and perturbed oxytocin signaling has been linked to the pathogenesis of several psychiatric disorders. However, it is still largely unknown how oxytocin exactly regulates neuronal function. We show that early, transient oxytocin exposure in vitro inhibits the development of hippocampal glutamatergic neurons, leading to reduced dendrite complexity, synapse density, and excitatory transmission, while sparing GABAergic neurons. Conversely, genetic elimination of oxytocin receptors increases the expression of protein components of excitatory synapses and excitatory synaptic transmission in vitro. In vivo, oxytocin-receptor-deficient hippocampal pyramidal neurons develop more complex dendrites, which leads to increased spine number and reduced g-oscillations. These results indicate that oxytocin controls the development of hippocampal excitatory neurons and contributes to the maintenance of a physiological excitation/inhibition balance, whose disruption can cause neurobehavioral disturbances.

    Original languageEnglish
    Article numbere22466
    JournaleLife
    Volume6
    DOIs
    Publication statusPublished - 2017 Feb 23

    ASJC Scopus subject areas

    • Neuroscience(all)
    • Biochemistry, Genetics and Molecular Biology(all)
    • Immunology and Microbiology(all)

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