Morphine causes a delayed increase in glutamate receptor functioning in the nucleus accumbens core
European Journal of Pharmacology , Volume 511 - Issue 1 p. 27- 30
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 α-amino-3-hydroxy-5-methyl- 4-isoxazole propionic acid (AMPA)-induced [3H]-γ-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.
|GABA release, Gene expression, Ionotropic glutamate receptor, Nucleus accumbens core|
|European Journal of Pharmacology|
|Organisation||Department of Molecular Genetics|
Jacobs, E.H, Wardeh, A.J, Smit, A.B, & Schoffelmeer, A.N.M. (2005). Morphine causes a delayed increase in glutamate receptor functioning in the nucleus accumbens core. European Journal of Pharmacology, 511(1), 27–30. doi:10.1016/j.ejphar.2005.02.009