μ and δ opioid synergy between the periaqueductal gray and the rostro-ventral medulla
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5.15 - The Brainstem and Nociceptive Modulation
2020, The Senses: A Comprehensive Reference: Volume 1-7, Second EditionInflammatory mediators of opioid tolerance: Implications for dependency and addiction
2019, PeptidesCitation Excerpt :Our results further suggest that solTNF mediates morphine tolerance in the PAG via TNFRI signaling and augmentation of glutamate homeostasis. Given that PAG-mediated analgesia depends largely on the ability of opioids to inhibit vlPAG MOR-expressing GABAergic neurons [12,19,22,39,43,47,65,162–186], our data suggest that TLR4 signaling contributes to opioid tolerance by decreasing the ability of morphine to hyperpolarize vlPAG GABAergic neurons, thereby maintaining tonic inhibition of vlPAG-RVM projections neurons, and preventing opioid analgesia. Glia modulation of opioid tolerance has been reported at every major level of the descending analgesic circuit: PAG, RVM, and spinal cord dorsal horn.
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2018, European Journal of PharmacologySigma 1 receptor: A new therapeutic target for pain
2013, European Journal of PharmacologyCitation Excerpt :Further experiments based on the selective blockade of σ1 receptor synthesis by the i.c.v. administration of specific antisense oligodeoxynucleotides confirmed the supraspinal location of the modulation of opioid analgesia (King et al., 1997; Pan et al., 1998; Mei and Pasternak, 2002). Several supraspinal brainstem structures have been involved in morphine analgesic activities and complex synergistic interactions among three morphine- sensitive sites have been described: the periaqueductal gray matter, the locus coeruleus, and the rostroventral medulla (Rossi et al., 1993, 1994). Although the σ1 receptor is expressed in these three gray areas (Walker et al., 1992; Alonso et al., 2000), the opioid potentiating activity largely differs depending on the site, as it has been reported by Mei and Pasternak (2007).