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The Journal of Neuroscience, March 15, 2002, 22(6):2335-2342

Lower Sensitivity to Stress and Altered Monoaminergic Neuronal Function in Mice Lacking the NMDA Receptor epsilon 4 Subunit

Yoshiaki Miyamoto1, Kiyofumi Yamada1, Yukihiro Noda1, Hisashi Mori2, Masayoshi Mishina2, and Toshitaka Nabeshima1

1 Department of Neuropsychopharmacology and Hospital Pharmacy, Nagoya University Graduate School of Medicine, Showa-ku, Nagoya 466-8560, Japan, and 2 Department of Molecular Neurobiology and Pharmacology, School of Medicine, University of Tokyo, Bunkyou-Ku, Tokyo 113-0033, Japan

NMDA receptors, an ionotropic subtype of glutamate receptors (GluRs), play an important role in excitatory neurotransmission, synaptic plasticity, and brain development. They are composed of the GluRzeta subunit (NR1) combined with any one of four GluRepsilon subunits (GluRepsilon 1-GluRepsilon 4; NR2A-NR2D). Although the GluRzeta subunit exists in the majority of the CNS throughout all stages of development, the GluRepsilon subunits are expressed in distinct temporal and spatial patterns. In the present study, we investigated neuronal functions in mice lacking the embryonic GluRepsilon 4 subunit. GluRepsilon 4 mutant mice exhibited reductions of [3H]MK-801 [(+)-5-methyl-10,11-dihydro-5H-dibenzo [a,d] cyclohepten-5,10-imine maleate] binding and 45Ca2+ uptake through the NMDA receptors. The expression of GluRzeta subunit protein, but not GluRepsilon 1 and GluRepsilon 2 subunit proteins, was reduced in the frontal cortex and striatum of the mutant mice. A postmortem examination in GluRepsilon 4 mutant mice revealed that tissue contents of norepinephrine, dopamine, serotonin, and their metabolites were reduced in the hippocampus and that dopamine, as well as serotonin, metabolism was upregulated in the frontal cortex, striatum, hippocampus, and thalamus. To clarify the phenotypical influences of the alteration in neuronal functions, performances in various behavioral tests were examined. GluRepsilon 4 mutant mice showed reduced spontaneous locomotor activity in a novel environment and less sensitivity to stress induced by the elevated plus-maze, light-dark box, and forced swimming tests. These findings suggest that GluRepsilon 4 mutant mice have dysfunctional NMDA receptors and altered emotional behavior probably caused by changes in monoaminergic neuronal activities in adulthood.

Key words: NMDA receptor; GluRepsilon 4 subunit; GluRzeta subunit; monoaminergic neuronal systems; locomotor activity; emotional behavior

Copyright © 2002 Society for Neuroscience  0270-6474/02/2262335-08$05.00/0


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