“Key regulatory effects of Oxytocin animal and human behavior include promotion of facial recognition and maternal nurturing, control of anxiety, and regulation of spatial memory.”


At delivery, an Oxt surge in the maternal bloodstream promotes labor and subsequent lactation. The circulating Oxt reaches the fetal brain, where it regulates the developmental switch of GABAergic signaling from excitation to inhibition…early blockade of Oxt signaling affects the development of synaptic wiring in the brain and leads to lifelong consequences, including neuropsychiatric diseases…

Oxt exerts an early and cell-type specific ’priming’ effect on developing excitatory neurons to regulate dendrite branching and synapse development, synaptic transmission, and the synchronicity of neuronal networks…Oxt exposure for 1–3 days only affects the morphology of excitatory hippocampal neurons…GABAergic neurons contain the intracellular signaling pathways that mediate the Oxt effects on neuronal morphology but are intrinsically insensitive to Oxt due to the lack of Oxtrs…The increased dendrite branching of excitatory neurons caused by deficient Oxt signaling likely leads to an increase in the balance between excitation and inhibition in neuronal networks, which might also ultimately be the cause of the increased seizure susceptibility of Oxtr-deficient mice. Such a disturbance in the excitation/inhibition balance has repeatedly been invoked as a causal contributor to ASD pathology…

Our results indicate that Oxt signaling exerts an early priming effect on developing glutamatergic neurons in the hippocampus. This process throttles dendrite development and thus guarantees a proper excitation/inhibition balance. Aberrations in this process, caused for instance by genetic perturbation of Oxt signaling, as shown here, or by deficient Oxt signaling during pregnancy, parturition, or early postnatal brain development, cause dendrite hypertrophy, an increased excitation/inhibition balance, and consequent defects in network synchrony in the hippocampus, and likely also in other brain regions. These findings provide important insights into the role of Oxt signaling in fetal and early postnatal brain development, and represent an explanatory basis for the etiological role that dysfunctions in Oxt signaling appear to play in ASDs and other neuropsychiatric disorders.


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