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Oxytocin suppresses basal glutamatergic transmission but facilitates activity‐dependent synaptic potentiation in the medial prefrontal cortex
Author(s) -
Ninan Ipe
Publication year - 2011
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07430.x
Subject(s) - neuroscience , glutamatergic , neurotransmission , oxytocin , oxytocin receptor , long term potentiation , synaptic plasticity , prefrontal cortex , glutamate receptor , metaplasticity , chemistry , psychology , medicine , receptor , cognition
J. Neurochem. (2011) 119 , 324–331. 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.