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. 2018 Nov 6;9:544. doi: 10.3389/fpsyt.2018.00544

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Copyright © 2018 Mei, Wu and Zhou.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The NMDAR hypofunction hypothesis proposes that NMDARs in inhibitory interneurons are preferentially diminished in schizophrenia. The reduced NMDAR function in interneurons (the left inset) results in decreased excitatory postsynaptic currents, which in turn decrease interneuron output (the right inset). The reduced GABA release from interneuron terminals leads to smaller inhibitory postsynaptic responses and thereby a disinhibition of postsynaptic excitatory neurons (the right inset). This finally leads to an enhanced output of excitatory neurons, resulting in excessive glutamate release and increased activation of non-NMDA glutamate receptors. This process might be enhanced by NMDAR antagonists and ameliorated by mGluR2/3 agonists.