Rat trigeminal lamina I neurons that project to thalamic or parabrachial nuclei contain the mu-opioid receptor.
Ligands of the mu-opioid receptor are known to inhibit nociceptive transmission in the dorsal horn, yet the cellular site(s) of action for this inhibition remain to be fully elucidated. Neurons located in lamina I of the dorsal horn are involved in distinct aspects of nociceptive transmission. Neurons projecting to the thalamus are thought to be involved in sensory-discriminative aspects of pain perception, while neurons projecting to the parabrachial nucleus are thought to be important for emotional and/or autonomic responses to noxious stimuli. The present study examined these two populations of lamina I projection neurons in the trigeminal dorsal horn to determine if the mu-opioid receptor protein (MOR1) is differentially located in these populations of neurons. Lamina I projection neurons were identified using the retrograde tracer FluoroGold (FGold). FGold was injected into either the contralateral thalamus (ventral posterolateral (VPM)/ventral posterolateral (VPL) thalamic region) or into the ipsilateral parabrachial nuclei. The distribution of MOR1 in these neurons was determined using immunocytochemistry. The distribution of MOR1-ir within these two populations of lamina I projection neurons was examined by both confocal and electron microscopy. We found that both populations of projection neurons contained MOR1. Immunogold analyses revealed the presence of MOR1-ir at membrane sites and within the cytoplasm of these neurons. Cytoplasmic receptor labeling may represent sites of synthesis, recycling or reserve populations of receptors. MOR1 was primarily found in the somata and proximal dendrites of projection neurons. In addition, these neurons rarely received synaptic input from MOR1-containing axon terminals. These results indicate that lamina I neurons in trigeminal dorsal horn that project to the thalamic and parabrachial nuclei contain MOR1 and are likely sites of action for MOR ligands that modulate sensory and/or autonomic aspects of pain transmission in the trigeminal dorsal horn.
Mitchell
J L
JL
Neurological Sciences Institute, Oregon Health and Science University, 505 Northwest 185(th) Avenue, Beaverton, OR 97006, USA.
Silverman
M B
MB
Aicher
S A
SA
D000818:Animals; D003712:Dendrites / Q000378:metabolism / Q000648:ultrastructure; D007150:Immunohistochemistry; D008297:Male; D046529:Microscopy, Electron, Transmission; D009434:Neural Pathways / Q000378:metabolism* / Q000648:ultrastructure; D018847:Opioid Peptides / Q000378:metabolism; D010146:Pain / Q000378:metabolism / Q000503:physiopathology; D011149:Pons / Q000378:metabolism* / Q000648:ultrastructure; D020671:Posterior Horn Cells / Q000378:metabolism* / Q000648:ultrastructure; D051381:Rats; D017207:Rats, Sprague-Dawley; D017450:Receptors, Opioid, mu / Q000378:metabolism*; D013266:Stilbamidines; D014275:Trigeminal Caudal Nucleus / Q000378:metabolism* / Q000648:ultrastructure; D020651:Ventral Thalamic Nuclei / Q000378:metabolism* / Q000648:ultrastructure
C049774:2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt; D018847:Opioid Peptides; D017450:Receptors, Opioid, mu; D013266:Stilbamidines