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  • Title: Rostrocaudal variation in targeting of N-methyl-D-aspartate and mu-opioid receptors in the rat medial nucleus of the solitary tract.
    Author: Huang J, Wang H, Pickel VM.
    Journal: J Comp Neurol; 2000 Jun 05; 421(3):400-11. PubMed ID: 10813795.
    Abstract:
    N-methyl-D-aspartate (NMDA) receptors and mu-opioid receptors (MOR) have been implicated in gustatory and cardiorespiratory visceral reflexes, respectively involving second order sensory neurons in rostral and intermediate portions of the medial nucleus of the solitary tract (mNTS). To determine whether there are cellular sites suggesting functional interaction involving NMDA receptors and MOR in these regions, we examined their ultrastructural immunocytochemical localization by using antisera recognizing the functional subunit of NMDA receptors (NR1) or MOR in rat brain. In both mNTS subdivisions, NR1 labeling was prominently seen along membranes of cytoplasmic organelles in somata and large dendrites, as well as on asymmetric postsynaptic densities in small dendrites and dendritic spines. Many of these profiles also contained MOR immunoreactivity that was mainly distributed along extrasynaptic plasma membranes. Quantitative regional comparison showed that dendrites composed 64% (167 of 261) and 35% (137 of 390) of the dually labeled structures in the rostral and intermediate mNTS, respectively. In contrast, only 11% (28 of 261) of the total dually labeled profiles in the rostral, but 46% (180 of 390) of those in the intermediate mNTS were axon terminals. Many of the terminals containing NR1 and/or MOR were large and formed asymmetric synapses with multiple targets, resembling those features of known visceral afferents. Our results suggest that opioids, active at MOR in mNTS, modulate excitatory visceral reflexes involving mainly postsynaptic NMDA receptors in the rostral region. In addition, they suggest that similar mechanisms exist in the intermediate mNTS, where both NMDA receptors and MOR may differentially regulate the presynaptic release of glutamate from the visceral afferents.
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