Plasmalemmal μ-opioid receptor distribution mainly in nondopaminergic neurons in the rat ventral tegmental area

Authors

  • Miguel Garzón,

    Corresponding author
    1. Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA
    2. Departamento de Morfología, Facultad de Medicina UAM, Madrid, 28029, Spain
    • Department of Neurology and Neuroscience, Cornell University Medical College, 411 E. 69th St., Room KB-410, New York, NY 10021
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  • Virginia M. Pickel

    1. Department of Neurology and Neuroscience, Cornell University Medical College, New York, New York 10021, USA
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Abstract

Opiate-evoked reward and motivated behaviors reflect, in part, the enhanced release of dopamine produced by activation of the μ-opioid receptor (μOR) in the ventral tegmental area (VTA). We examined the functional sites for μOR activation and potential interactions with dopaminergic neurons within the rat VTA by using electron microscopy for the immunocytochemical localization of antipeptide antisera raised against μOR and tyrosine hydroxylase (TH), the synthesizing enzyme for catecholamines. The cellular and subcellular distribution of μOR was remarkably similar in the two major VTA subdivisions, the paranigral (VTApn) and parabrachial (VTApb) nuclei. In each region, somatodendritic profiles comprised over 50% of the labeled structures. μOR immunolabeling was often seen at extrasynaptic/perisynaptic sites on dendritic plasma membranes, and 10% of these dendrites contained TH. μOR-immunoreactivity was also localized to plasma membranes of axon terminals and small unmyelinated axons, none of which contained TH. The μOR-immunoreactive axon terminals formed either symmetric or asymmetric synapses that are typically associated with inhibitory and excitatory amino acid transmitters. Their targets included unlabeled (30%), μOR-labeled (25%), and TH-labeled (45%) dendrites. Our results suggest that μOR agonists in the VTA affect dopaminergic transmission mainly indirectly through changes in the postsynaptic responsivity and/or presynaptic release from neurons containing other neurotransmitters. They also indicate, however, that μOR agonists directly affect a small population of dopaminergic neurons expressing μOR on their dendrites in VTA and/or terminals in target regions. Synapse 41:311–328, 2001. © 2001 Wiley-Liss, Inc.

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