4.7 Article

Morphine causes a delayed increase in glutamate receptor functioning in the nucleus accumbens core

Journal

EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 511, Issue 1, Pages 27-30

Publisher

ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2005.02.009

Keywords

ionotropic glutamate receptor; gene expression; GABA release; nucleus accumbens core

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Enhanced excitatory neurotransmission in the mesocorticolimbic system may contribute to the persistence of addiction behaviour. Here, we demonstrated that glutamate-, N-methyl-D-aspartate (NMDA)- and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA)-induced [H-3]-gamma-aminobutyric acid (GABA) release from superfused rat nucleus accumbens core slices is profoundly enhanced 3 weeks, but not 3 days, after a single s.c. morphine injection. This delayed increase in glutamate receptor functioning is associated with enhanced gene transcript levels of ionotropic NMDA and AMPA/kainate receptor subunits. These data reveal that morphine may progressively enhance glutamate neurotransmission within the nucleus accumbens core subsequent to drug exposure. (c) 2005 Elsevier B.V. All rights reserved.

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