Microinjections of glutamate or morphine at coincident midbrain sites have different effects on nociceptive dorsal horn neurons in the rat
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Ventrolateral Periaqueductal Gray Matter Neurochemical Lesion Facilitates Epileptogenesis and Enhances Pain Sensitivity in Epileptic Rats
2019, NeuroscienceCitation Excerpt :In contrast, inhibition of glutamatergic transmission, or activation of GABAergic transmission, in vlPAG facilitates nociception (Samineni et al., 2017). Early studies have shown that microinjection of glutamate receptor agonists or gamma-aminobutyric acid (GABA) antagonists into the vlPAG produces antinociceptive effect (Moreau and Fields, 1986; Ness and Gebhart, 1987; Carstens et al., 1988; Jones and Gebhart, 1988; Sandkuhler et al., 1989; Carstens et al., 1990; Budai and Fields, 1998; Morgan et al., 2003). In contrast, microinjection of glutamate receptor antagonists or GABA agonists into the vlPAG produces hyperalgesia (Moreau and Fields, 1986; Depaulis et al., 1987; Siegfried and de Souza, 1989; Behbehani et al., 1990).
Inflammatory 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.
Unmasking the mysteries of the habenula in pain and analgesia
2012, Progress in NeurobiologyCitation Excerpt :Morphine acts directly on habenula neurons to produce analgesia (Zhou et al., 1981; Cohen and Melzack, 1985). Such information clearly implicates an analgesic effect that is observed when morphine is directly injected into other brain structures including the cingulate cortex (LaGraize et al., 2006) and the periaqueductal gray (Carstens et al., 1988; Bernal et al., 2007). While it can inhibit and facilitate excitatory synaptic transmission (Hashimoto et al., 2009), how it affects analgesia through direct action on the habenula is unclear, but assumed to be through activation of brainstem modulatory systems.