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Prolonged exposure to NMDAR antagonist induces cell-type specific changes of glutamatergic receptors in rat prefrontal cortex
Journal article   Open access   Peer reviewed

Prolonged exposure to NMDAR antagonist induces cell-type specific changes of glutamatergic receptors in rat prefrontal cortex

Huai-Xing Wang and Wen-Jun Gao
Neuropharmacology, v 62(4), pp 1808-1822
Mar 2012
PMID: 22182778
url
https://doi.org/10.1016/j.neuropharm.2011.11.024View
Published, Version of Record (VoR) Open

Abstract

Pyramidal Cells - cytology Receptors, N-Methyl-D-Aspartate - antagonists & inhibitors Interneurons - drug effects Rats Excitatory Amino Acid Antagonists - pharmacology Miniature Postsynaptic Potentials - drug effects Prefrontal Cortex - cytology Excitatory Postsynaptic Potentials - drug effects Rats, Sprague-Dawley Animals Prefrontal Cortex - drug effects Female Synaptic Transmission - drug effects Interneurons - cytology Pyramidal Cells - drug effects Dizocilpine Maleate - pharmacology Action Potentials - drug effects
N-methyl-d-aspartic acid (NMDA) receptors are critical for both normal brain functions and the pathogenesis of schizophrenia. We investigated the functional changes of glutamatergic receptors in the pyramidal cells and fast-spiking (FS) interneurons in the adolescent rat prefrontal cortex in MK-801 model of schizophrenia. We found that although both pyramidal cells and FS interneurons were affected by in vivo subchronic blockade of NMDA receptors, MK-801 induced distinct changes in α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and NMDA receptors in the FS interneurons compared with pyramidal cells. Specifically, the amplitude, but not the frequency, of AMPA-mediated miniature excitatory postsynaptic currents (mEPSCs) in FS interneurons was significantly decreased whereas both the frequency and amplitude in pyramidal neurons were increased. In addition, MK-801-induced new presynaptic NMDA receptors were detected in the glutamatergic terminals targeting pyramidal neurons but not FS interneurons. MK-801 also induced distinct alterations in FS interneurons but not in pyramidal neurons, including significantly decreased rectification index and increased calcium permeability. These data suggest a distinct cell-type specific and homeostatic synaptic scaling and redistribution of AMPA and NMDA receptors in response to the subchronic blockade of NMDA receptors and thus provide a direct mechanistic explanation for the NMDA hypofunction hypothesis that have long been proposed for the schizophrenia pathophysiology.

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