Characterization of functional μ opioid receptor turnover in rat locus coeruleus: an electrophysiological and immunocytochemical study.

After near-complete, irreversible μ receptor inactivation with β–funaltrexamine (β-FNA), opioid effect spontaneously recovered in a rapid and efficaciousmanner. In contrast, α2-adrenoceptor-mediated effect hardly recovered after receptor inactivation with the irreversible antagonist EEDQ. When the r...

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Detalles Bibliográficos
Autores: Medrano Muñoz, María Carmen, Santamarta, María Teresa, Pablos Laría, Inés Patricia, Aira Muga, Zigor, Buesa Sobera, Itxaso, Azkue Barrenetxea, Jon Jatsu, Mendiguren Ordorica, Aitziber, Pineda Ortiz, Joseba Gotzon
Tipo de recurso: artículo
Fecha de publicación:2017
País:España
Institución:Universidad del País Vasco
Repositorio:Addi. Archivo Digital para la Docencia y la Investigación
OAI Identifier:oai:addi.ehu.eus:10810/74905
Acceso en línea:http://hdl.handle.net/10810/74905
Access Level:acceso abierto
Palabra clave:opioid tolerance
μ receptors
noradrenergic nucleus
locus coeruleus
Descripción
Sumario:After near-complete, irreversible μ receptor inactivation with β–funaltrexamine (β-FNA), opioid effect spontaneously recovered in a rapid and efficaciousmanner. In contrast, α2-adrenoceptor-mediated effect hardly recovered after receptor inactivation with the irreversible antagonist EEDQ. When the recovery of opioid effect was tested after various inactivating time schedules, we found that the longer the β-FNA pre exposure, the less efficient and slower the functional μ receptor turnover became. Interestingly, μ receptor turnover was slower when β-FNA challenge was repeated in the same cell, indicating constitutive μ receptor recycling by trafficking from a depletable pool. Double immunocytochemistry confirmed the constitutive nature of μ receptor trafficking from a cytoplasmic compartment. The μ receptor turnover was slowed down when LC neuron calcium- or firing-dependent processes were prevented or vesicular protein trafficking was blocked by a low temperature or transport inhibitor.