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Acute morphine associated alterations in the subcellular location of the AMPA-GluR1 receptor subunit in dendrites of neurons in the mouse central nucleus of the amygdala: Comparisons and contrasts with other glutamate receptor subunits


Correspondence to: Michael J. Glass, Brain and Mind Research Institute, Weill Cornell Medical College, New York, New York 10065. E-mail:


Within the amygdala, AMPA receptors expressing the AMPA-GluR1 (GluR1) subunit play an important role in basal glutamate signaling as well as behaviors associated with exposure to drugs of abuse like opiates. Although the ultrastructural location of GluR1 is an important functional feature of this protein, the basal distribution of GluR1, as well as its sensitivity to acute morphine, has never been characterized in the mouse central nucleus of the amygdala (CeA). Electron microscopic immunocytochemistry employing visually distinct gold and peroxidase markers was used to explore the distribution of GluR1 and its relationship with the mu-opioid receptor (µOR) in the mouse CeA under basal conditions and after morphine. We also looked at the effect of morphine on other glutamate receptor subunits, including AMPA-GluR2 (GluR2) and NMDA-NR1 (NR1). In opiate naive animals, GluR1 and µOR were present in diverse populations of neuronal profiles, but mainly in somatodendritic structures that expressed exclusive labeling for either antigen, as well as those co-expressing both proteins. Compared to saline treated animals, mice given morphine showed significant differences in the subcellular location of GluR1 in dendrites without co-expression of µOR. Although GluR2 also showed similar changes in non-µOR expressing dendrites, contrasting effects were seen in GluR2 and µOR co-expressing profiles. These results provide the ultrastructural basis for basal interactions involving the modulation of GluR1 or µOR activity in the mouse CeA. Further, they indicate that the subcellular distribution of GluR1 is modified by acute opiates in a manner that compares, as well as contrasts, with GluR2. Synapse 67:692–704, 2013. © 2013 Wiley Periodicals, Inc.