Cited by 110Neuroendocrine regulation and behaviorNeuroscience and Neuropharmacology ResearchNeurotransmitter Receptor Influence on Behavior

Oxytocin suppresses basal glutamatergic transmission but facilitates activity-dependent synaptic potentiation in the medial prefrontal cortex

Ninan, Ipe·2011·Journal of Neurochemistry

Abstract

Both oxytocin and oxytocin receptors are implicated in neuropsychiatric disorders, particularly autism which involves a severe deficit in social cognition. Consistently, oxytocin enhances social cognition in humans and animals. The infralimbic medial prefrontal cortex (IL-mPFC) is believed to play an important role in the regulation of social cognition which might involve top-down control of subcortical structures including the amygdala. However, little is known about whether and how oxytocin modulates synaptic function in the IL-mPFC. The effect of oxytocin on excitatory neurotransmission in the IL-mPFC was studied by examining both the evoked and spontaneous excitatory neurotransmission in the IL-mPFC layer V pyramidal neurons before and after perfusion with oxytocin. To investigate the effect of oxytocin on synaptic plasticity, low-frequency stimulation-induced long-lasting depression was studied in oxytocin-treated brain slices. Oxytocin produced a significant suppression of glutamatergic neurotransmission in the IL-mPFC layer V pyramidal neurons which was mediated by a reduction in glutamate release. Activation of the cannabinoid CB1 receptors was involved in this pre-synaptic effect. Treatment of brain slices with oxytocin for 1 h converted long-lasting depression into long-lasting potentiation of glutamatergic neurotransmission. This oxytocin-mediated plasticity was NMDA receptor-dependent and was mediated by the synaptic insertion of calcium-permeable α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors. The aforementioned suppression of basal glutamatergic neurotransmission and facilitation of activity-dependent synaptic plasticity in the IL-mPFC might be critical for the effect of oxytocin on social cognition.

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Crossref · 10.1111/j.1471-4159.2011.07430.x

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Authors
Ninan, I.
Affiliations
NYU Langone Health (US)
Corresponding author
Ninan, Ipe
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2011-09-20
Volume
119
Issue
2
Pages
324-331
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
OpenAlex
W1879824241
Cited by
110
References
69
Citations by year
2026: 6 · 2025: 3 · 2024: 7 · 2023: 4 · 2022: 7 · 2021: 7 · 2020: 9 · 2019: 7 · 2018: 11 · 2017: 12 · 2016: 3 · 2015: 7 · 2014: 11 · 2013: 11 · 2012: 4
FWCI
11.71
Type
journal article
Language
en
Open access
closed
Locations
  • Journal of Neurochemistry (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Social Sciences › Psychology › Social Psychology › Neuroendocrine regulation and behavior
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
oxytocin, medial prefrontal cortex, infralimbic cortex, glutamatergic neurotransmission, synaptic plasticity, layer 5 pyramidal neurons, glutamate release, CB1 receptor, NMDA receptor, calcium-permeable AMPA receptors, social cognition, autism spectrum disorder, oxytocin receptor
MeSH terms
Animals, Dose-Response Relationship, Drug, Female, Male, Mice, Inbred C57BL, Synaptic Transmission, Neuronal Plasticity, Oxytocin, Synapses, Prefrontal Cortex, Pyramidal Cells, Receptors, Oxytocin, Receptors, AMPA, Neurotransmitter Agents, Glutamic Acid, Excitatory Postsynaptic Potentials, Receptor, Cannabinoid, CB1, Mice, Electrophysiological Phenomena, In Vitro Techniques

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